Master of Science, University of Akron, 2009, Biology

The immune system is responsible for protecting the body from disease by identifying by destroying pathogenic microorganisms, materials and even dangerous self-cells. This protection is carried out by specialized cells which are found in the bone marrow, circulating blood, thymus, lymph nodes, spleen, as well as other lymphatic tissues. These cells each carry out specific functions and convey different types of protection. Modulation of the balance of either the number or functionality of these immune cells can lead to immune deficiency, susceptibility to disease, or autoimmune disorders such as chronic inflammation. A number of studies have shown that the immune system can be affected by both physical and psychological stresses, such as depression and post-traumatic stress disorder (PTSD). In the present study we examined immune status in women victims of intimate partner violence (IPV). Immune system parameters measured included both immune cell counts as well as functionality of the cells. The results indicated that victims of IPV who suffered from depression and PTSD showed significantly higher baseline activity of natural killer (NK) cells and decreased change in NK cell activity when stimulated with heat shock protein 60 (HSP60). This drop in reactivity to a typical cellular stress signal could put PTSD positive IPV victims at risk for a number of diseases, including cancer development and viral infection. Also, an increased basal activity of NK cells could indicate an autoimmune pathology. These results may lead to a better understanding of the health issues associated with IPV, PTSD, and depression, and will hopefully assist in the development of better and more complete therapies.

Committee: James Holda PhD (Advisor) Subjects: Biology; Health; Immunology; Psychobiology; Womens Studies

MS, University of Cincinnati, 2020, Education, Criminal Justice, and Human Services: Information Technology

Internet of things (IoT) applications in our daily lives has made life easier, but also comes with associated security threats. The vulnerability of the IoT system stems from the vulnerability of each connected device and transmission of threats through an interconnected home network. Smart homes are one of the applications of IoT, which is comprised of connected devices for easier interaction. An isolated IoT system with no internet connection has some level of safety from attacks because it is not exposed to the internet, although these devices have their innate vulnerabilities from the manufacturer. IoT gateways connecting IoT devices to the internet can create a backdoor into the smart home system that an attacker can exploit. Therefore, Internet-connected IoT devices have a high-security risk and one of the ways to detect an intrusion into an IoT gateway is through anomalies in the traffic passing through it. This thesis introduces early work on an intrusion detection system (IDS) by detecting anomalies in the smart home network using Extreme Learning Machine and Artificial Immune System (AIS-ELM). AIS uses the Clonal Algorithm for the optimization of the input parameters, and ELM analyzes the input parameter for better convergence in detecting anomalous activity. The larger implications of this work are the potential to apply this approach to a smart home network gateway and combine it with a push notification system that will allow the homeowner to identify any abnormalities in the smart home network and take appropriate action to mitigate threats.

Committee: Nelly Elsayed Ph.D. (Committee Chair); Jess Kropczynski Ph.D. (Committee Chair); Shane Halse Ph.D. (Committee Member) Subjects: Information Technology

MS, Kent State University, 2007, College of Arts and Sciences / Department of Computer Science

Immune System is essential for the survival of the species. How exactly this sophisticated defense mechanism accomplishes the level of discrimination remains deeply enigmatic. Both Immune System and Intrusion Detection System work toward a comparable goal, identifying and responding to malicious agents. The effectiveness of an Intrusion Detection System however, depends on its ability to accurately differentiate between an event and an incident. Today computer scientists and researchers are borrowing some of the underlying principles of Immunology to implement such a system. The Human Immune System primarily involves highly specific recognition of foreign antigens and tolerance of self antigens. For more than six decades, the concept of ‘self / non-self' formed the central theme of Immunology. The model states that all foreign entities that are not part of the organism trigger an immune response, whereas self elements do not. In the last few years, several researchers have challenged the authenticity of this concept and have come up with rival ideas. One such notion is the Danger Theory for Immunology. According to this new viewpoint, the Immune System does not discriminate between self and non-self elements but between danger and non-danger. Danger is perceived as a signal emitted by the cells that die an unnatural death. Detection of a foreign entity occurs in conjunction with the detection of danger signals which are emanated as a result of discontinuity in the constant interactions between the immune receptors and their targets. In this thesis, the author proposes a new Danger Theory based Event-Incident Model for Intrusion Detection System. The proposed model also borrows some key characteristics of autonomous multi-agent system. It employs a group of detectors known as the ‘Mobile Intrusion Detection Squad' and utilizes the ‘Divide and Conquer Approach' to identify and respond to both distributed and coordinated attacks. The literature of Immune-based Intrusio (open full item for complete abstract)

Committee: Michael Rothstein (Advisor) Subjects: Computer Science

Doctor of Philosophy in Engineering, University of Toledo, 2012, College of Engineering

The probabilistic reliability evaluation of power systems is a complex and highly dimensional problem that often requires a large amount of computational resources, particularly processing power and time. The complexity of this problem is only increasing with the advent of the smart grid and its accompanying technologies, such as plug-in hybrid electric vehicles (PHEVs). Such technologies, while they add convenience, intelligence, and reduce environmental impacts, also add dynamic and stochastic loads that challenge the current reliability and security of the power grid. One method that is often used to evaluate the reliability of power systems is Monte Carlo simulation (MCS). As the complexity and dimensionality of a power system grows, MCS requires more and more resources leading to longer computational times. Multiple methods have previously been developed that aid in reducing the computational resources necessary for MCS in order to achieve a more efficient and timely convergence while continuing to accurately assess the reliability of a given system. Examples include analytical state space decomposition, population based metaheuristic algorithms (PBMs), and the use of high performance computing (HPC). In order to address these issues, this dissertation is focused on improving the performance of algorithms used to examine the level of reliability in composite power systems through the use of computational intelligence (CI) and HPC, while also investigating the impact of PHEVs on the power grid at the composite and distribution levels. Contributions include the development and exploration of 3 variations of a new, hybrid algorithm called intelligent state space pruning (ISSP) that combines PBMs with non-sequential MCS in order to intelligently decompose, or prune, a given state space and improve computational efficiency, an evaluation of the use of latin hypercube sampling and low discrepancy sequences in place of MCS, the use of serial and parallel support vecto (open full item for complete abstract)

Committee: Lingfeng Wang Ph.D. (Committee Chair); Mansoor Alam Ph.D. (Committee Co-Chair); Jackson Carvalho Ph.D. (Committee Member); Vijay Devabhaktuni Ph.D. (Committee Member); Mohsin Jamali Ph.D. (Committee Member); Weiqing Sun Ph.D. (Committee Member) Subjects: Artificial Intelligence; Computer Science; Electrical Engineering

Doctor of Philosophy, The Ohio State University, 2023, Biomedical Sciences

CD4+ T cells are a subset of the adaptive immune response that are classically defined as “helper” type cells, responsible for aiding in the effective recruitment and function of other immune cells. In addition to these traditional helper type roles, however, an additional subset of CD4+ T cells characterized by the ability to perform cytotoxic functions classically attributed to Nature Killer (NK) and CD8+ T cells, has emerged. This additional subset, deemed CD4+ cytotoxic T lymphocytes (CD4-CTLs), produce cytolytic effector molecules and directly kill compromised cells in a major histocompatibility complex class-II (MHC-II) restricted fashion. While initially thought to be a bi-product of in vitro culturing, CD4-CTLs have now been identified in a broad range of both human and murine immune responses. Specifically, CD4-CTLs have been shown to play largely protective roles in numerous antitumor and antiviral responses, including those to influenza and SARS-CoV-2. Conversely, dysregulated CD4-CTLs have been implicated in the pathogenesis of autoimmune diseases, including multiple sclerosis and ulcerative colitis. Despite their documented importance in a wide range of immunological contexts, the mechanisms that underly their differentiation and function remain enigmatic. Here, we first identify the Ikaros Zinc Finger transcription factor Aiolos (encodedby Ikzf3) as a reciprocal regulator of CD4-CTL and T-follicular helper (TFH) cell populations. TFH cells represent a classical CD4+ T helper cell populations that, upon activation and subset specific differentiation, interact with and provide aid to B-cells in the production of high-affinity neutralizing antibodies. In this work, we utilized a murine model of influenza infection, an immunologic context in which both TFH and CD4-CTLs have been shown to play important protective roles. We find that the absence of Aiolos resulted in global disruptions in TFH cell programming, including decreases in key transcription fa (open full item for complete abstract)

Committee: Ken Oestreich (Advisor); Hazem Ghoneim (Committee Chair); Thomas Mace (Committee Member); Murugesan Rajaram (Committee Member); Purnima Dubey (Committee Member) Subjects: Biomedical Research; Immunology

Doctor of Philosophy (PhD), University of Toledo, 2022, Biomedical Sciences (Medical Microbiology and Immunology)

Withheld at author's request

Committee: R. Mark Wooten Ph.D. (Advisor); Viviana Ferreira D.V.M., Ph.D. (Committee Member); Matam Vijay-Kumar Ph.D. (Committee Member); Randall Worth Ph.D. (Committee Member); Robert Blumenthal Ph.D. (Committee Member) Subjects: Biology; Biomedical Research; Experiments; Health Sciences; Immunology; Microbiology

Doctor of Philosophy (PhD), University of Toledo, 2020, Biomedical Sciences (Medical Microbiology and Immunology)

Sepsis is a process of severe immune dysregulation resulting from pathogenic disruption of immune homeostasis, leading to damage of multiple organ systems and high mortality. Case-fatality rates range from 10% to 60% or higher, with $24 billion spent yearly on sepsis in the United States alone. In addition, organ damage and continued immune insufficiency require hospital readmission in nearly 50% of severe sepsis survivors within 6 months. Current symptomatic treatments, while effective to a certain degree even in cases of severe sepsis, do not address the mechanisms of sepsis or prevent complications in survivors. Immunosuppressive treatments also fail to address the dysregulation that causes sepsis, and may increase the rate of metabolic and cardiovascular issues after treatment is completed. Utilizing a novel drug-screening method, we have found that retinoic acid (RA) significantly upregulates the anti-inflammatory protein MAP kinase phosphatase 1 (MKP-1). Our experiments show that RA has significant beneficial effects on both sepsis and endotoxemia. RA, which is used to treat diverse diseases due to its ability to re-regulate the immune system, significantly reduces morbidity and mortality of early sepsis in two mouse models. RA, when administered in a true bacterial sepsis model, significantly reduces mortality by 75% in mice, and significantly reduces both visible lung damage and neutrophil infiltration into the lungs. Levels of pro-inflammatory cytokines are reduced in mouse organs and serum, indicating systemic pro-regulatory effects. In addition, RA significantly reduces pro-inflammatory cell signaling, downregulating the transcription, translation, and/or translocation into the nucleus of pro-inflammatory proteins in human and mouse cells. While the mechanisms of these effects are as yet unknown, we hypothesize that RA functions through binding to MKP-1 and other regulatory proteins, and thus exerts anti-inflammatory and pro-differentiation effec (open full item for complete abstract)

Committee: Stanislaw Stepkowski (Committee Chair); Zhixing K. Pan (Committee Member); R. Mark Wooten (Committee Member); Saurabh Chattopadhyay (Committee Member); Randall Worth (Committee Member) Subjects: Biomedical Research; Immunology

Master of Arts, The Ohio State University, 2019, Psychology

Disgust is an emotional experience that tends to shape the way individuals perceive their worlds. The more chronically disgusted an individual is, the more likely they are to come to view their worlds as a dangerous place. There are times, however, when individuals must chose to approach or avoid potentially disgusting ambiguous stimuli. For example, seeing someone sneeze on the bus could be categorized as either very dangerous (i.e. has the potential for infection) or relatively benign (i.e. was caused by a harmless source such as seasonal allergies). The current research explores how fundamental individual differences in valence weighting bias – a cognitive process in which known positive attitudes and known-negative attitudes are generalized to the appraisal of a novel or ambiguous stimulus – affects pathogen disgust and the view that the world is a dangerous place. In Study 1, the evidence suggests that pathogen disgust is correlated with valence weighting bias such that individuals with a negative valence weighting bias were more likely to be sensitive to pathogen disgust. Valence weighting bias was also indirectly associated with dangerous world beliefs (DWB) through pathogen disgust. Study 2 sought evidence for the causal effects of valence weighting bias on DWB. In the control condition, when using pathogen disgust to approximate valence weighting bias, the conventional pattern between disgust and DWB was found. Those that were pathogenically disgust sensitive also believed that the world was a dangerous place. When valence weighting biases were manipulated through an experimental procedure that recalibrates individuals' weighting tendencies toward a more balanced and objectively appropriate weighting of positive and negative valence, the relation between disgust sensitivity and DWB was significantly attenuated. Thus it appears that valence weighting bias plays a role in how individuals come to perceive our worlds. Taken together, the results of this (open full item for complete abstract)

Committee: Russell Fazio Ph.D (Advisor); Richard Petty Ph.D (Committee Member); Baldwin Way Ph.D (Committee Member) Subjects: Psychology

Doctor of Philosophy, Case Western Reserve University, 2017, Pathology

HCV-infection affects approximately 170 million worldwide, with 60-85 percent of acute-infections resulting in chronic-infection, and a significant proportion are co-infected with HIV. HCV-infection causes increased morbidity and mortality in HCV-HIV co-infection. HIV-infection alters HCV-disease pathogenesis, accelerating progression to cirrhosis and liver failure. While HCV-therapy has greatly improved, the cost remains a barrier and is not expected to completely remove HCV from the population. We need a better understanding of the immune-response to HCV to develop successful vaccine strategies. HCV-containment and -clearance is dependent on efforts of the innate and adaptive immune-response. CD4 memory T-cells are critical in viral-clearance, by producing IFN¿ and mediating CD8 T-cell responses. NK cells have been shown to exert an important role in control of HCV-infection by lysis of infected-cells and cytokine release. Monocytes may partly shape this HCV-directed response, via direct-contact with CD4 T-cells and NK cells and in production of soluble factors. IL-7 has been demonstrated to enhance NK cell IFN¿ production, and the IL-7 receptor a chain (CD127) is expressed on NK cells. We measured CD127 expression on NK cell subsets of uninfected donors, chronic HCV-infected treatment-naive, HIV-infected on ART and HCV-HIV co-infected subjects on ART. We demonstrate that CD56bright NK cell CD127 expression negatively correlated with HCV plasma levels in HCV mono-infection and HCV-HIV co-infection. We observed IL-7-induced NK cell activation, cell-cycling, IFN¿ release and cytolytic function, with impairments in HCV- and HIV-infections. These findings offer a role for IL-7-dependent NK cell function in control of chronic viral infections. Within chronic HCV- and HIV-infection, there have been observations of elevated levels of IL-6 and sCD14, produced in part by monocytes, which contribute to immune-activation. We extended these studies to evaluate th (open full item for complete abstract)

Committee: Donald Anthony MD, PhD (Advisor); Dave Canaday MD (Committee Chair); Scott Sieg PhD (Committee Member); Daniel Popkin MD, PhD (Committee Member); Clive Hamlin PhD (Committee Member) Subjects: Immunology

Doctor of Philosophy, Case Western Reserve University, 2015, Pharmacology

Cdk5 is a unique member of a family of serine/threonine cyclin-dependent kinases. Although Cdk5 is ubiquitously expressed, this kinase is predominantly active in post-mitotic neurons where there is abundant expression of its obligate activating partners p35 and/or p39. Consequently, Cdk5 has been historically considered a `neuron-specific' kinase and recognized as an essential regulator of neuronal functions. However, aberrant Cdk5 activity has be associated with a variety of inflammatory neurodegenerative disorders and activity of the Cdk5-p35 complex has been associated with disorders involving non-neuronal tissues, indicating the potential for novel extra-neuronal roles for Cdk5. Our work describes a previously unknown function of the Cdk5-p35 complex in T cells. We demonstrate the activity of Cdk5 is required for the induction of EAE, a T-cell-mediated neuro-inflammatory disease model of multiple sclerosis. Activation of T cells leads to an induction of Cdk5-p35 expression that we show is essential for optimal T cell function. In an effort to define mechanisms mediating this effect of Cdk5, we discovered that Cdk5 controls IL2 gene expression during T-cell activation by modulating the HDAC1/mSin3a repressor complex. We show this effect of Cdk5 is dependent on specific phosphorylation of the mSin3a protein at serine 861. Disruption of Cdk5 activity in T cells results in enhanced HDAC activity and binding of the HDAC1/mSin3a repressor complex to the IL2 promoter and subsequently leads to the suppression of IL2 expression. In our pursuit of alternative mechanisms, we focused on Foxp3+ regulatory T cells (Tregs) whose activity is essential for maintaining immune homeostasis and controlling inflammation in the CNS. We show that Cdk5 activity is a determinant of the expression of Foxp3 in CD4+ T cells, effectively regulating the differentiation of Tregs in the presence of pro-inflammatory factors. Our data show the IL-6 induced repression of Foxp3 gene ex (open full item for complete abstract)

Committee: John Letterio MD (Advisor); Noa Noy PhD (Committee Chair); Bing-Cheng Wang PhD (Committee Member); Anthony Berdis PhD (Committee Member); Marvin Nieman PhD (Committee Member) Subjects: Cellular Biology; Immunology; Molecular Biology

Doctor of Philosophy, The Ohio State University, 2014, Neuroscience Graduate Studies Program

Aging is associated with the development of primed and hyper-reactive microglial population within the central nervous system (CNS). After an immune challenge these primed microglia release exaggerated levels of inflammatory cytokines into the CNS resulting in the development of neuropsychological complications including cognitive decline and depression. How and why these primed microglia develop in the aged brain is unclear, but recent studies indicate that microglia in the aged brain have reduced exposure and are more resistant to anti-inflammatory regulation. Rather than impairment in a single regulatory pathway, the aged brain demonstrates a loss in almost every regulatory system investigated including neuronal regulation by CD200 and fractalkine (CX3CL1), anti-inflammatory regulation by interleukin (IL)-10 and IL-4, and global regulation by micro-RNAs (miRs). Of these regulatory pathways, research into mechanisms for reduced CX3CL1 expression, reduced responsiveness to IL-4, and aberrant miR expression in the aged brain is lacking. Moreover, research into the degree to which the development of this primed microglia phenotype can be accelerated by CNS trauma or the degree to which primed microglia contribute to neuropsychiatric complications experienced by persons with traumatic brain injury (TBI) has not been performed. To address these holes in our understanding of microglia regulation and priming in the aged and injured CNS four primary studies were performed. In the first study, miRs associated with the immune response were measured in adult and aged mouse and human brain, and mouse microglia. In both mouse and human samples miR-29a/b-1 was significantly increased with age associated with reduced expression of CX3CL1 and insulin-like growth factor (IGF)-1, two confirmed targets of miR-29a/b-1 that negatively regulate microglia activation. Thus, age-associated increases in miR-29a/b-1 could contribute to reduced microglial regulation and the developmen (open full item for complete abstract)

Committee: Jonathan Godbout Dr. (Advisor); Phillip Popovich Dr. (Committee Member); Amy Lovett-Racke Dr. (Committee Member); Daniel Eiferman Dr. (Committee Member); John Sheridan Dr. (Committee Member) Subjects: Aging; Immunology; Neurosciences

Doctor of Philosophy, The Ohio State University, 2013, Microbiology

Listeria monocytogenes is a facultative intracellular pathogen that infects a large variety of host cells, including macrophages and diverse non-phagocytic cells. To avoid the phagosome microbicidal environment, L. monocytogenes secretes a pore-forming toxin (listeriolysin O; LLO) that releases the bacterium into the cytoplasm. Once in the cytosol, L. monocytogenes proliferates and infects adjacent cells through cell-to-cell spreading. Innate immune cells like neutrophils play an important role in the control of infection, yet the interaction between neutrophils, other host cells, and L. monocytogenes is not well understood. Neutrophils produce a high concentration and variety of antimicrobial molecules, including defensins and proteases; thus it is likely that these cells enhance the anti-listerial response of other host cells. This dissertation addresses if: i) human defensins, which can be released into the extracellular milieu by neutrophils, enable macrophages to control intracellular replication of L. monocytogenes; ii) L. monocytogenes is able to replicate in human neutrophils in a LLO-dependent manner as observed in macrophages; and iii) human neutrophils cooperate with macrophages to prevent L. monocytogenes replication in human macrophages. Addressing i), we found that the alpha-defensin HNP-1 (one of the most abundant proteins in neutrophil primary granules) cooperates with macrophages to inhibit L. monocytogenes phagosomal escape and intracellular growth. Importantly, HNP-1 is acquired by macrophages and trafficked to the phagocytosed bacteria. Finally, HNP-1 inhibits LLO secretion from the bacteria and directly blocks LLO activity. In conclusion, neutrophil defensins inhibit LLO function through two mechanisms (secretion and activity), and inhibit L. monocytogenes escape from macrophage phagosomes. Addressing ii), we found that LLO enhances the phagocytic efficiency of neutrophils and does not protect L. monocytogenes from neutrophil intracellular ki (open full item for complete abstract)

Committee: Stephanie Seveau (Advisor) Subjects: Cellular Biology; Immunology; Microbiology

MS, University of Cincinnati, 2001, Medicine : Environmental Health Sciences

Jet fuel is a common occupational exposure among commercial and military maintenance workers. JP-8 jet fuel, a military formulation, has been found to have immunotoxic effects in mice but little data exists for humans. The aim of this cross-sectional study was to determine if the number of immune cells in the peripheral blood was altered among tank entry workers, a group which has been determined in previous studies to have the highest exposure to JP-8 in the U.S Air Force. A total of 123 volunteers (45 tank entry workers) from three Air Force bases participated in the study. After adjusting for a number of covariates, tank entry workers were found to have higher numbers of white blood cells (p=0.01), neutrophils (p=0.05), and monocytes (p=0.02) and no differences in the numbers of total lymphocytes, T-cells, T-helper cells, T-suppressor cells, Natural Killer cells, and B-cells when compared with a low exposure group. Tank entry workers did not show any clinical effects of the increased immune cell counts. Although there were no differences in the number of lymphocytes among study groups, further investigations are needed to evaluate the functional ability of these cells to produce lymphokines and cytokines and modulate the immune system.

Committee: Grace Lemasters (Advisor) Subjects:

PhD, University of Cincinnati, 2005, Medicine : Molecular and Cellular Physiology

Lysozyme is an abundant, cationic antimicrobial protein that plays an important role in pulmonary host defense. Increased concentration of lysozyme in the airspaces of transgenic mice enhanced bacterial killing whereas lysozyme deficiency resulted in increased bacterial burden and morbidity. Lysozyme degrades peptidoglycan in the bacterial cell wall leading to rapid killing of Gram-positive organisms; however, this mechanism cannot account for the protective effect of lysozyme against Gram-negative bacteria following infection of transgenic mice. The current study was therefore designed to test the hypothesis that the catalytic activity (muramidase activity) of lysozyme is not required for bacterial killing in vivo. Substitution of serine for aspartic acid at position 53 (D53S) in mouse lysozyme M completely ablated muramidase activity. Muramidase-deficient recombinant lysozyme (LysMD53S) killed both Gram-positive and Gram-negative bacteria in vitro. Targeted expression of LysMD53S in the respiratory epithelium of wild type (LysM+/+/LysMD53S) or lysozyme M null mice (LysM-/-/LysMD53S) resulted in elevated lysozyme protein in the airspaces without any increase in muramidase activity. Intratracheal challenge of transgenic mice with Gram-positive or Gram-negative bacteria resulted in a significant increase in bacterial burden in LysM-/-mice that was completely reversed by targeted expression of LysMD53S. These results indicate that the muramidase activity of lysozyme is not essential for bacterial killing in vitro or in vivo.

Committee: Dr. Timothy Weaver (Advisor) Subjects:

Doctor of Philosophy, University of Toledo, 2011, Mathematics

HIV is a virus currently affecting approximately 33.3 million people worldwide. Since it's discovery in the early 1980s, researchers have strived to find treatment that helps the immune system eradicate the virus from the human body. A great deal of advances have been made in helping HIV infected individuals from advancing to AIDS, but no cure has yet been found. Researchers have found that the immune system is in a chronic state of activation during HIV infection and believe this could be a major contributor to the decline of immune system cell populations. Using analysis of systems of Ordinary Differential Equations, this paper serves to better understand the dynamics of the activated immune system during HIV infection. Both current and possible future therapies are considered.

Committee: H. Westcott Vayo PhD (Advisor); Joana Chakraborty PhD (Committee Member); Marianty Ionel PhD (Committee Member); Denis White PhD (Committee Member) Subjects: Biomedical Research; Mathematics; Medicine

Master of Science, Miami University, 2012, Zoology

The immune system is critical to an animal's survival. However, changes in immune function during insect development, and the factors that regulate these changes, are not well understood. Hemocytes carry out cellular defenses such as phagocytosis, nodulation, and encapsulation of pathogens. The enzyme phenoloxidase (PO) plays a key role in this process while the enzyme lysozyme breaks down bacterial cell walls. Total PO (TPA) and lysozyme activities, total blood hemocytes, and encapsulation ability were examined from late nymphal stages through early adulthood in the cricket, Acheta domesticus. TPA increased with age while encapsulation ability tended to decrease. The effects of crowding and light stress during nymphal development on adult immune parameters were determined. Crowding increased TPA in crickets housed in small but not large groups. Light stress negatively impacted survival, but not immune function. Further investigation of the effects of early life stress on adult immune function is thus warranted.

Committee: Kathleen A. Killian PhD (Advisor); Nancy G. Solomon PhD (Committee Member); Ann L. Rypstra PhD (Committee Member) Subjects: