T Lymphocyte Polyclonal Proliferation and Stress Response Style

1987 ◽  
Vol 60 (3_part_2) ◽  
pp. 1121-1122
Author(s):  
Edward A. Workman ◽  
Mariano F. La Via
Keyword(s):  
T Cell ◽  
T Lymphocyte ◽  
Life Stress ◽  
Type A Behavior ◽  
Response Style ◽  
Cell Mediated Immunity ◽  
Behavioral Indices ◽  
Cell Immunity ◽  
Stress Avoidance ◽  
Pearson Correlations

18 subjects were measured on cell-mediated immunity (T lymphocyte polyclonal proliferation) and four behavioral indices including over-all life stress, stress-avoidance tendency, stress-intrusion tendency, and tendency toward cardiovascular Type A behavior. Of Pearson correlations computed between T lymphocyte polyclonal proliferation and each of the four behavioral indices, the only significant value was that, .47, between T cell immunity and tendency toward stress avoidance. Of the variables investigated, the best predictor of T cell immunocompetence is the tendency toward avoiding stress. Results are discussed in terms of implications for research.

scholarly journals T Cell Immunity and the Quest for Protective Vaccines against Staphylococcus aureus Infection

2020 ◽  
Vol 8 (12) ◽  
pp. 1936
Author(s):  
Erin Armentrout ◽  
George Liu ◽  
Gislâine Martins
Keyword(s):  
Staphylococcus Aureus ◽  
T Cell ◽  
Vaccine Trial ◽  
Preventive Measure ◽  
T Cell Subsets ◽  
Cell Mediated Immunity ◽  
Mortality And Morbidity ◽  
Aureus Infection ◽  
Cell Immunity ◽  
Causative Agents

Staphylococcus aureus is a wide-spread human pathogen, and one of the top causative agents of nosocomial infections. The prevalence of antibiotic-resistant S. aureus strains, which are associated with higher mortality and morbidity rates than antibiotic-susceptible strains, is increasing around the world. Vaccination would be an effective preventive measure against S. aureus infection, but to date, every vaccine developed has failed in clinical trials, despite inducing robust antibody responses. These results suggest that induction of humoral immunity does not suffice to confer protection against the infection. Evidence from studies in murine models and in patients with immune defects support a role of T cell-mediated immunity in protective responses against S. aureus. Here, we review the current understanding of the mechanisms underlying adaptive immunity to S. aureus infections and discuss these findings in light of the recent S. aureus vaccine trial failures. We make the case for the need to develop anti-S. aureus vaccines that can specifically elicit robust and durable protective memory T cell subsets.

scholarly journals Lack of CD4+ T Cells Does Not Affect Induction of CD8+ T-Cell Immunity against Encephalitozoon cuniculi Infection

2000 ◽  
Vol 68 (11) ◽  
pp. 6223-6232 ◽  
Author(s):  
Magali Moretto ◽  
Lori Casciotti ◽  
Brigit Durell ◽  
Imtiaz A. Khan
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Response ◽  
T Cell Response ◽  
T Cell Immunity ◽  
Cell Mediated Immunity ◽  
Wild Type ◽  
Encephalitozoon Cuniculi ◽  
Cell Immunity ◽  
Mouse Tissues

ABSTRACT Cell-mediated immunity has been reported to play an important role in defense against Encephalitozoon cuniculi infection. Previous studies from our laboratory have underlined the importance of cytotoxic CD8+ T lymphocytes (CTL) in survival of mice infected with E. cuniculi. In the present study, immune response against E. cuniculi infection in CD4+T-cell-deficient mice was evaluated. Similar to resistant wild-type animals, CD4−/− mice were able to resolve E. cuniculi infection even at a very high challenge dose (5 × 107 spores/mouse). Tissues from infected CD4−/− mice did not exhibit higher parasite loads in comparison to the parental wild-type mice. Conversely, at day 21 postinfection, susceptible CD8−/− mice had 1014 times more parasites in the liver compared to control wild-type mice. Induction of the CD8+ T-cell response in CD4−/− mice against E. cuniculi infection was studied. Interestingly, a normal antigen-specific CD8+T-cell response to E. cuniculi infection was observed in CD4−/− mice (precursor proliferation frequency, 1/2.5 × 104 versus 1/104 in wild-type controls). Lack of CD4+ T cells did not alter the magnitude of the antigen-specific CTL response (precursor CTL frequency; 1/1.4 × 104 in CD4−/− mice versus 1/3 × 104 in control mice). Adoptive transfer of immune CD8+ T cells from both CD4−/− and wild-type animals prevented the mortality in CD8−/− mice.E. cuniculi infection thus offers an example of an intracellular parasitic infection where CD8+ T-cell immunity can be induced in the absence of CD4+ T cells.

scholarly journals Polymeric Pathogen-Like Particles-Based Combination Adjuvants Elicit Potent Mucosal T Cell Immunity to Influenza A Virus

2021 ◽  
Vol 11 ◽  
Author(s):  
Brock Kingstad-Bakke ◽  
Randall Toy ◽  
Woojong Lee ◽  
Pallab Pradhan ◽  
Gabriela Vogel ◽  
...  
Keyword(s):  
T Cells ◽  
Influenza Virus ◽  
T Cell ◽  
Influenza A ◽  
Memory T Cells ◽  
T Cell Immunity ◽  
Cell Mediated Immunity ◽  
Tlr Agonists ◽  
Cell Immunity ◽  
Resident Memory T Cells

Eliciting durable and protective T cell-mediated immunity in the respiratory mucosa remains a significant challenge. Polylactic-co-glycolic acid (PLGA)-based cationic pathogen-like particles (PLPs) loaded with TLR agonists mimic biophysical properties of microbes and hence, simulate pathogen-pattern recognition receptor interactions to safely and effectively stimulate innate immune responses. We generated micro particle PLPs loaded with TLR4 (glucopyranosyl lipid adjuvant, GLA) or TLR9 (CpG) agonists, and formulated them with and without a mucosal delivery enhancing carbomer-based nanoemulsion adjuvant (ADJ). These adjuvants delivered intranasally to mice elicited high numbers of influenza nucleoprotein (NP)-specific CD8+ and CD4+ effector and tissue-resident memory T cells (TRMs) in lungs and airways. PLPs delivering TLR4 versus TLR9 agonists drove phenotypically and functionally distinct populations of effector and memory T cells. While PLPs loaded with CpG or GLA provided immunity, combining the adjuvanticity of PLP-GLA and ADJ markedly enhanced the development of airway and lung TRMs and CD4 and CD8 T cell-dependent immunity to influenza virus. Further, balanced CD8 (Tc1/Tc17) and CD4 (Th1/Th17) recall responses were linked to effective influenza virus control. These studies provide mechanistic insights into vaccine-induced pulmonary T cell immunity and pave the way for the development of a universal influenza and SARS-CoV-2 vaccines.

scholarly journals T lymphocyte colony assay in hemophiliacs

Blood ◽  
1984 ◽  
Vol 64 (1) ◽  
pp. 105-109
Author(s):  
MV Ragni ◽  
A Winkelstein ◽  
TL Evans ◽  
JH Lewis ◽  
FA Bontempo ◽  
...  
Keyword(s):  
T Cell ◽  
T Lymphocyte ◽  
Interleukin 2 ◽  
Immune Deficiency Syndrome ◽  
Risk Groups ◽  
Cell Contact ◽  
Cell Mediated Immunity ◽  
Minimal Cell ◽  
Colony Assay

Unexplained lymphadenopathy, with or without accompanying symptoms, known as the “lymphadenopathy syndrome,” has been recognized in groups at risk for acquired immune deficiency syndrome (AIDS), namely, homosexuals and hemophiliacs. To date, however, no test has been defined that discriminates between asymptomatic individuals and those with adenopathy in these high-risk groups. The T colony assay, which measures T lymphocyte growth in soft agar and which allows selective T cell proliferation with minimal cell-cell contact, was evaluated in asymptomatic hemophiliacs. Significantly lower mean colony counts were found in eight hemophiliacs with adenopathy (HA), 763 +/- 348 (+/- SEM), than in 16 healthy hemophiliacs (HH) 3,044 +/- 661 (P less than .005), or than in 24 heterosexual control subjects, 3,964 +/- 395 (P less than .005). The in vitro addition of exogenous interleukin-2 (IL- 2) restored normal colony growth in the HA population. These results indicate that the T colony assay can detect abnormal cell-mediated immunity among hemophiliacs and specifically discriminates between asymptomatic hemophiliacs (HH) and those with adenopathy (HA). In addition, IL-2 may be of potential benefit in improving T cell defects in AIDS or the “lymphadenopathy syndrome”; however, this remains to be proven.

T-lymphocyte maturation abnormalities in uninfected newborns and children with vertical exposure to HIV

Blood ◽  
2000 ◽  
Vol 96 (12) ◽  
pp. 3866-3871 ◽  
Author(s):  
Mario Clerici ◽  
Marina Saresella ◽  
Fulvia Colombo ◽  
Sabrina Fossati ◽  
Natascia Sala ◽  
...  
Keyword(s):  
T Cell ◽  
T Lymphocyte ◽  
Cell Maturation ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cell Mediated Immunity ◽  
Older Children ◽  
Clinical Events ◽  
Hiv Women ◽  
T Cell Maturation ◽  
Hiv Negative

Abstract Cell-mediated immunity and T-lymphocyte maturation are impaired in HIV-infected children. These abnormalities would be detected in HIV-uninfected offspring of HIV women (seroreverters [SR]) if HIV or its soluble proteins could cross the placental barrier. Immunophenotypic analyses were performed in 20 healthy HIV-uninfected newborns of HIV-infected mothers (SR), and in 14 healthy newborns of HIV-negative women (UC). The same analyses were performed in 3 groups of older children: SR (n = 41); UC (n = 15); and HIV-infected children (n = 25). Antigen-specific cells were evaluated with ELISpot and fluorimetric analyses; IL-7 serum concentration was measured by enzyme-linked immunosorbent assay (ELISA). Results showed that in SR newborns: (1) the CD4/CD8 ratio was reduced, (2) CD4+ and CD8+ naive T-cell percentages were decreased, (3) percentage of activated CD8+ T cells was increased, and (4) percentages of CD3+/4−/8− (DN) and DN/25−/44+ were augmented. These abnormalities were partially retained in older SR children. CD4+ and CD8+ HIV-specific cells were detected in a portion of newborn SRs but not in older SRs. Serum IL-7 was augmented both in newborn and older SRs. Cell-mediated immunity and T-cell maturation are altered even in HIV-uninfected newborns of HIV-infected mothers; these abnormalities persist over time. The biologic significance of these observations and potential subsequent clinical events should be investigated in larger cohorts of seroreverters.

scholarly journals T-lymphocyte-enriched murine peritoneal exudate cells. IV. Genetic control of cross-stimulation at the T-cell level.

1977 ◽  
Vol 145 (2) ◽  
pp. 327-343 ◽  
Author(s):  
R H Schwartz ◽  
C L Horton ◽  
W E Paul
Keyword(s):  
T Cell ◽  
T Lymphocyte ◽  
Peritoneal Exudate ◽  
The Other ◽  
Mouse Strains ◽  
Cell Level ◽  
Cross Reactions ◽  
Cell Immunity ◽  
The Cross ◽  
Branched Chain

Antibodies raised against many structurally related antigens have been shown to cross-react extensively. Manifestations of T-cell immunity, on the other hand, appear to be more restricted in their ability to be elicited by cross-reacting antigens, although examples have been reported. This paper explores the nature of the cross-reactions at the T-cell level among the branched-chain copolymers (T,G)-A--L, (phi,G)-A--L, (H,G)-A--L, and G-A--L, as well as a related linear terpolymer, GAT, in a variety of mouse strains using the peritoneal exudate T-lymphocyte-enriched cells (PETLES) proliferation assay. (T,G)-A--L, (phi,G)-A--L, and GAT could cross-stimulate cells immune to the other two antigens, whereas (H,G)-A--L, (T,G)-Pro--L, and G-A--L showed no cross-stimulations. The extent of the cross-reactions varied with the mouse strain and was shown to be under the control of immune response genes. It was necessary for the strain to be able to respond to both the immunogen and the cross-reacting antigen, when used as an immunogen, in order for cross-stimulation to occur; however, this was not always sufficient. Several examples of unequal or one-way cross-reactions were found. In addition, the immune responses to (H,G)-A--L and (phi,G)-A--L showed no cross-reactions with the other antigen even though their Ir genes were both mapped to the K region or I-A subregion. The problem of accounting for such fine specificity of T-cell recognition in lieu of the genetic evidence demonstrating only Ir gene control of the response is discussed.

scholarly journals Selection of macrophage-resistant progressor tumor variants by the normal host. Requirement for concomitant T cell-mediated immunity.

1983 ◽  
Vol 157 (2) ◽  
pp. 642-656 ◽  
Author(s):  
J L Urban ◽  
H Schreiber
Keyword(s):  
T Cell ◽  
Tumor Antigen ◽  
Specific Antigen ◽  
High Sensitivity ◽  
Immune Defense ◽  
Growth Potential ◽  
Cell Mediated Immunity ◽  
Cell Immunity

The ultraviolet radiation-induced fibrosarcoma 1591 is generally rejected by normal syngeneic mice, but occasionally the tumor succeeds in growing progressively. Analysis of these progressively growing tumors has regularly demonstrated the development of tumor variants that have acquired a heritable progressive growth potential. We have analyzed the phenotypic changes of these variants to determine which kind of selection pressure had occurred during the evolution of the variants, thus giving insight into the relative importance and hierarchy of the different immune defense mechanisms that may be operating in normal individuals as a defense against neoplastic cells. We discovered that all of the host-selected progressor variants had lost not only a strong T cell-recognized and tumor-specific antigen, but also their high sensitivity to cytotoxic macrophages. No selection for macrophage-resistance or loss of the tumor antigen was observed in 1591 tumors reisolated from idiotypically-suppressed mice or from other mice lacking tumor-specific T cell immunity. Analysis of other tumor variants selected in vitro showed that 1591 tumor cells have the potential to lose sensitivity to tumoricidal macrophages without losing the T cell-recognized tumor antigen. Thus the data suggest that T cells and macrophages act together to suppress the outgrowth of potentially malignant cells in vivo.

Inhibition of T lymphocyte heparanase by heparin prevents T cell migration and T cell-mediated immunity

1990 ◽  
Vol 20 (3) ◽  
pp. 493-499 ◽  
Author(s):  
Ofer Lider ◽  
Yoseph A. Mekori ◽  
Ted Miller ◽  
Ruth Bar-Tana ◽  
Israel Vlodavsky ◽  
...  
Keyword(s):  
Cell Migration ◽  
T Cell ◽  
T Lymphocyte ◽  
Cell Mediated Immunity ◽  
T Cell Migration

scholarly journals Btn2a2, a T cell immunomodulatory molecule coregulated with MHC class II genes

2016 ◽  
Vol 213 (2) ◽  
pp. 177-187 ◽  
Author(s):  
Kerstin Sarter ◽  
Elisa Leimgruber ◽  
Florian Gobet ◽  
Vishal Agrawal ◽  
Isabelle Dunand-Sauthier ◽  
...  
Keyword(s):  
T Cell ◽  
Mhc Class Ii ◽  
Class Ii ◽  
Cell Mediated Immunity ◽  
Factor X ◽  
Cell Immunity ◽  
Cell Induction ◽  
Genes Encoding ◽  
Inhibitory Molecule ◽  
Antigen Presenting

Evidence has recently emerged that butyrophilins, which are members of the extended B7 family of co-stimulatory molecules, have diverse functions in the immune system. We found that the human and mouse genes encoding butyrophilin-2A2 (BTN2A2) are regulated by the class II trans-activator and regulatory factor X, two transcription factors dedicated to major histocompatibility complex class II expression, suggesting a role in T cell immunity. To address this, we generated Btn2a2-deficient mice. Btn2a2−/− mice exhibited enhanced effector CD4+ and CD8+ T cell responses, impaired CD4+ regulatory T cell induction, potentiated antitumor responses, and exacerbated experimental autoimmune encephalomyelitis. Altered immune responses were attributed to Btn2a2 deficiency in antigen-presenting cells rather than T cells or nonhematopoietic cells. These results provide the first genetic evidence that BTN2A2 is a co-inhibitory molecule that modulates T cell–mediated immunity.

514 Disturbed Mitochondrial Dynamics Rewire the Epigenetic Program for CD8+ TIL Exhaustion

2020 ◽  
Vol 8 (Suppl 3) ◽  
pp. A550-A550
Author(s):  
Yi-Ru Yu ◽  
Haiping Wang ◽  
Fabien Franco ◽  
Ping-Chih Ho
Keyword(s):  
T Cells ◽  
T Cell ◽  
De Novo ◽  
Mitochondrial Dynamics ◽  
Glucose Deprivation ◽  
Cell Mediated Immunity ◽  
T Cell Exhaustion ◽  
Cell Exhaustion ◽  
Cell Immunity

BackgroundCancer immunotherapy, including checkpoint blockade and adoptive transfer of tumor-reactive T cells, represents a paradigm shift in the treatment of malignancies in recent years, and yields remarkable responses by reawakening anti-tumor immunity in established tumors. Nevertheless, a significant portion of patients are refractory to cancer immunotherapies, which may be in part due to the persistent impairment of anti-tumor effector functions in T cells, a phenomenon referred to as T cell exhaustion. Emerging evidence reveal that alterations in global chromatin accessibility and de novo DNA methylation patterns are keys events to drive development of T cell exhaustion under chronic antigenic stresses. However, it remains elusive how T cells engage epigenetic reprogramming to orchestrate exhausted state.MethodsHere, we examined the mitochondrial fitness in CD8+ TILs with mitoTrackers.ResultsWe found that tumor-infiltrating tumor-reactive T cells with accumulation of damaged mitochondria, characterized by increased mitochondrial mass but reduced mitochondrial membrane potential and cristae, display more severe exhausted phenotypes, including decreased proliferation capacity, reduced cytokine production and up-regulation of co-inhibitory receptors. The accumulation of damaged mitochondria is in part due to the deficiency of mitophagy machinery. Importantly, we found that the accumulation of dysfunctional mitochondria is corelated to the specificity and affinity of antigen, and also supported by the PD-1 expression. Moreover, the combination of glucose deprivation, hypoxia and TCR signaling in vitro can drastically weaken T cell immunity with the accumulation of dysfunctional mitochondria as seen in TILs previously. Furthermore, T cells with accumulation of damaged mitochondria, generated artificially by Oligomycin A and Mdivi-1, also exhibit persistent exhaustion features. Ultimately, supplementation with nicotinamide riboside enhances T cell mitochondrial fitness and improved responsiveness to anti-PD-1 treatment.ConclusionsTaken together, our study suggests that mitochondrial fitness is pivotal for T cell-mediated immunity and the accumulation of dysfunctional mitochondria could result in exhaustion phenotypes in T cells. And our findings also provide pillars for better harnessing T cell immune responses with metabolic regulations for immunotherapy.

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