scholarly journals T Cell Immunity to Bacterial Pathogens: Mechanisms of Immune Control and Bacterial Evasion

2020 ◽  
Vol 21 (17) ◽  
pp. 6144 ◽  
Author(s):  
Freya R. Shepherd ◽  
James E. McLaren
Keyword(s):  
T Cells ◽  
T Cell ◽  
Immune Responses ◽  
Pathogenic Bacteria ◽  
Bacterial Pathogens ◽  
Bacterial Species ◽  
Immune Defense ◽  
T Cell Immunity ◽  
Cell Immunity ◽  
Bacterial Antigens

The human body frequently encounters harmful bacterial pathogens and employs immune defense mechanisms designed to counteract such pathogenic assault. In the adaptive immune system, major histocompatibility complex (MHC)-restricted αβ T cells, along with unconventional αβ or γδ T cells, respond to bacterial antigens to orchestrate persisting protective immune responses and generate immunological memory. Research in the past ten years accelerated our knowledge of how T cells recognize bacterial antigens and how many bacterial species have evolved mechanisms to evade host antimicrobial immune responses. Such escape mechanisms act to corrupt the crosstalk between innate and adaptive immunity, potentially tipping the balance of host immune responses toward pathological rather than protective. This review examines the latest developments in our knowledge of how T cell immunity responds to bacterial pathogens and evaluates some of the mechanisms that pathogenic bacteria use to evade such T cell immunosurveillance, to promote virulence and survival in the host.

scholarly journals P04.06 mucosal immunization with a cDC1-targeted CTA1 adjuvant vaccine confers protection against melanoma metastasis

2020 ◽  
Vol 8 (Suppl 2) ◽  
pp. A39.1-A39
Author(s):  
M Arabpour ◽  
S Paul ◽  
R Kiffin ◽  
HG Wiktorin ◽  
K Hellstrand ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Immune Responses ◽  
Pulmonary Metastases ◽  
T Cell Immunity ◽  
Metastasis Formation ◽  
Mhc I ◽  
Mhc Ii ◽  
Cell Immunity

BackgroundSpecific targeting of anti-cancer vaccines to dendritic cells (DCs) has been shown to mount efficient immune responses against tumor cells. Classical CD103+dendritic cells (also called cDC1) have an inherent ability to cross-present antigens to CD8+ cytotoxic T cells. Here we have explored an anti-tumor vaccine that specifically targets cDC1 cells for protection against and elimination of metastatic melanoma. The vaccine contains the cholera toxin A1 subunit (CTA1) adjuvant and is targeted to cDC1 cells through an anti-CD103 single chain antibody (CD103 scFv).Material and MethodsC57BL/6 mice were injected with wild type or ovalbumin (OVA) expressing B16 melanoma cells either subcutaneously (s.c.) to establish solid tumors, or intravenously (i.v.) to allow the formation of pulmonary metastases. Before or after establishment of tumors, mice were intra-nasally inoculated with a vaccine composed of a CD103 scFv element fused to the adjuvant CTA1 and the MHC I H2kd-restricted OVA epitope SIINFEKL together with the MHC II H2kd-restricted OVA epitope p323 or just the p323 peptide alone (i.e. CTA1-SIINFEKL-p323-CD103 and CTA1-p323-CD103, respectively). Control mice were inoculated with PBS. The growth of solid tumors was carefully monitored and the development of pulmonary metastases was determined 2–3 weeks after tumor cell injection. In addition, antigen-specific T cell immunity following intranasal immunization was evaluated.ResultsTargeting MHC I and MHC II tumor cell epitopes to cDC1, via CD103 ScFv, in conjunction with the CTA1 adjuvant elicited strong tumor specific and protective CD8+ T cell responses as well as CD4+ T cell immunity. Immunization with the CTA1-SIINFEKL-p323-CD103 vaccine significantly reduced the growth of established solid B16F1-OVA melanomas (P<0.001) and potently prevented metastasis formation (P<0.01). Control immunizations with the CTA1-p323-CD103 vaccine tended to reduce metastasis, but tumor-specific CD8+ T cells were required for full therapeutic protection.ConclusionTargeting tumor specific CD8+ T cell epitopes to cDC1, in the context of a powerful adjuvant such as CTA1, leads to the development of efficient anti-tumor immune responses. Our results point towards the utility of cDC1-targeted vaccines in the treatment of established tumors or as a means to prevent metastasis formation.Disclosure InformationM. Arabpour: None. S. Paul: None. R. Kiffin: None. H.G. Wiktorin: None. K. Hellstrand: None. N. Lycke: None. A. Martner: None.

Despite Absence of Measurable Immune Responses against Adenovirus in the First 100 Days After Unrelated Umbilical Cord Blood Transplant in Vitro amplification Strategies Can Unveil Hexon and Penton-Specific Immunity.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 4640-4640
Author(s):  
Ann M. Leen ◽  
Anne Christin ◽  
Luciana C Marti ◽  
Jennifer H Baker ◽  
Paul Szabolcs
Keyword(s):  
T Cells ◽  
T Cell ◽  
Immune Responses ◽  
Cord Blood ◽  
Antiviral Immunity ◽  
T Cell Immunity ◽  
Cell Frequency ◽  
Post Transplant ◽  
Cell Immunity

Abstract Abstract 4640 Unrelated cord blood transplantation (UCBT) has become a life saving modality of hematopoietic cell transplantation (HCT) for those cancer patients who lack HLA-matched sibling donors. However, success after UCBT is limited by the high incidence of opportunistic infections (OI), most of which are viral and typically detected < 3 months after UCBT. A minority of UCBT patients with evidence of viral infection/reactivation post-transplant actually resolve their disease without antiviral therapy. Since these infections are largely controlled by T-cell immunity this suggests that in vivo T-cell priming may occur despite immunosuppressive drugs and functional T-cell deficits and protective antiviral immunity can be attained once a threshold number of antiviral T-cells have been achieved. To determine whether this was the case we collected PBMCs from 10 UCBT patients who underwent myeloablative regimens and were diagnosed with adenovirus infection (defined as positive PCR at least twice and/or viral culture in blood and/or stool and/or nasopharynx). Samples were collected a median of 88 days (range 37-209 days) post-transplant at first indication of Adv positivity (blood PCR + in 5/10 patients at a mean of ∼110,000 copies/ml, median of 350, range 100-1×106 copies/ml, 4 patients positive in stool only, one patient + in respiratory tract only). The median age of patients was 4.6 years (range 2.0-16.6y). Eight (8) out of ten (10) patients had grade 2-4 acute GVHD prior to the studies, while the other two patients had grade I. At baseline we were consistently unable to detect T-cells with reactivity against the immunodominant adenoviral virion proteins hexon and penton by IFN-g ELIspot [hexon - median 1.75 spot forming cells (SFC)/2×105 PBMC (range 1-12.5), penton – median 1 SFC)/2×105 PBMC (range 0.5-1)], even though the patients had evidence of active adenovirus infections. However, in 5/10 patients adenovirus-specific T cells could be amplified by a single in vitro stimulation with donor-derived mononuclear cells transduced with a recombinant adenovirus type 5 vector pseudotyped with a type 35 fiber (MOI 200 virus particles (vp) per cell) and culture in the presence of IL4 (1000u/ml). The median hexon-specific T cell frequency in the reactivated cytotoxic T lymphocyte (CTL) lines was 62.5 SFC/2×105 (range 34.5-299.5), and in one patient hexon epitope mapping revealed reactivity against at least four distinct peptides. Penton was also recognized by the CTL lines with a median T-cell frequency of 30 SFC/2×105 (range 26.5-164), with no recognition of control pepmixes. In contrast we were unable to expand adenovirus-reactive T cells from the remaining five patients. Two of three patients with positive ELIspot results from the CTL cultures against both hexon and penton are alive and adenovirus negative without any antiviral agents used at a median of 446 days post-UCBT (range 422-470). Four (4) patients died despite receiving antiviral treatment with Cidofovir. Two of these patients had no detectable antiviral immunity, while the others had only restricted or weak reactivity (reactivity against only one antigen or reactivity below the median SFC values of the responder cohort). To our knowledge this is the first study that analyzes the anti-adenoviral immune response in UCBT recipients with active infection in the early post-transplant period. It appears that in the first 100 days after UCBT, during a time of active immunosuppression, adenovirus-specific T-cells in peripheral blood are consistently (10/10 patients) below the level of detection of conventional IFN-g ELIspot assays. However, dormant immune responses can be amplified in vitro using a single stimulation in the presence of IL4. Furthermore, detection of functional CTL against hexon and penton proteins may be a useful marker to distinguish between those with effective antiviral T cell immunity and those at risk of developing progressive disease. Disclosures: No relevant conflicts of interest to declare.

DAPK2 and PIM1 Are Myeloma-Associated Antigens That Elicit Coordinated B and T Cell Immunity After Syngeneic HSCT.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 2445-2445
Author(s):  
Melinda Biernacki ◽  
Anselmo Alonso ◽  
Guanglan Zhang ◽  
Li Zhang ◽  
Wandi Zhang ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Immune Responses ◽  
Mhc Class I ◽  
Antibody Responses ◽  
T Cell Immunity ◽  
Class I ◽  
Molecular Remission ◽  
Tumor Associated Antigens ◽  
Cell Immunity

Abstract Abstract 2445 Poster Board II-422 Syngeneic hematopoietic stem cell transplantation (HSCT) can produce long-term disease-free survival in patients with hematologic malignancies, including multiple myeloma (MM). Because donor and host are genotypically identical in this setting, allo-immunity is absent and curative responses may result from donor-derived immune responses against tumor-associated antigens. We recently described potent, antigen-specific humoral immune responses arising after myeloablative syngeneic HSCT in an HLA-A2 positive patient with MM who achieved sustained molecular remission lasting over 3 years. Two target antigens of this response, DAPK2 and PIM1, were identified by serologic screening of a recombinant protein array consisting of the expressed products of 8000 open reading frames. Both proteins elicited antigen-specific antibody responses after HSCT that peaked around 3 months post-HSCT and gradually waned thereafter; prior to HSCT these antibody responses were low to undetectable. DAPK2 is a serine-threonine kinase involved in pro-apoptotic signaling, while PIM1 is an oncogene with known associations to B cell malignancies. By Western blot, both proteins demonstrate enriched protein expression in primary myeloma bone marrow compared to normal hematopoietic tissues. In the current studies, we determined whether antibody responses to DAPK2 and PIM1 were coordinated with T cell immunity against the same proteins following HSCT in this patient. As this patient was HLA-A2 positive, we used established MHC class I peptide binding algorithms to predict candidate peptide epitopes derived from PIM1 and DAPK2. We identified 23 9-mer peptides derived from DAPK2 and PIM1, all with high binding rank scores. All peptides were confirmed to bind to HLA-A2 using T2 binding assays. Ex vivo stimulation of fresh patient PBMC obtained ∼2.5 years post-HSCT with candidate peptides revealed 2 peptides, DAPK2156–164 (MLLDKNIPI) and PIM1191-199 (ALLKDTVYT) that elicited strong interferon-γ (IFNγ) secretion consistent with recall responses to these antigens. By IFNγ ELISpot, DAPK2- and PIM1-specific T cells recognized HLA-A2-positive myeloma cell lines MC/CAR and IM9, but not A2-negative OPM1 and NCI4929 lines. T cell recognition was mediated by CD8+ effector cells and was effectively blocked by the MHC class I blocking antibody w6/32. These studies indicate that the predicted peptides are naturally processed and presented by myeloma cells. When tested against CD138+ sorted primary MM marrow cells by IFNγ ELISpot, DAPK2-specific T cells and PIM1-specific T cells recognized 3 of 5 and 1 of 5 A2-positive primary tumor samples, respectively. Neither A2-negative CD138+ tumor samples nor A2-positive normal marrow elicited reactivity from antigen-specific T cells. These data demonstrate that PIM1 and DAPK2 are MM-associated antigens that commonly generate processed epitopes on malignant MM cells. Both proteins elicited coordinated B and T cell immunity in a MM patient who achieved sustained molecular remission after syngeneic HSCT. These data suggest that donor-derived MM-specific adaptive immunity contributes to disease regression following syngeneic HSCT for MM. As PIM1 and DAPK2 represent immunogenic tumor-associated antigens and not allo-antigens, these may be attractive targets for immunotherapy directed at MM outside of the context of allogeneic HSCT. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Reduced immune-regulatory molecule expression on human colonic memory CD4 T cells in older adults

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Stephanie M. Dillon ◽  
Tezha A. Thompson ◽  
Allison J. Christians ◽  
Martin D. McCarter ◽  
Cara C. Wilson
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd8 T Cells ◽  
Cd4 T Cells ◽  
Older Persons ◽  
Age Groups ◽  
T Cell Immunity ◽  
Cd4 T Cell ◽  
Cell Immunity ◽  
Memory Cd4 T Cells

Abstract Background The etiology of the low-level chronic inflammatory state associated with aging is likely multifactorial, but a number of animal and human studies have implicated a functional decline of the gastrointestinal immune system as a potential driver. Gut tissue-resident memory T cells play critical roles in mediating protective immunity and in maintaining gut homeostasis, yet few studies have investigated the effect of aging on human gut T cell immunity. To determine if aging impacted CD4 T cell immunity in the human large intestine, we utilized multi-color flow cytometry to measure colonic lamina propria (LP) CD4 T cell frequencies and immune-modulatory marker expression in younger (mean ± SEM: 38 ± 1.5 yrs) and older (77 ± 1.6 yrs) adults. To determine cellular specificity, we evaluated colon LP CD8 T cell frequency and phenotype in the same donors. To probe tissue specificity, we evaluated the same panel of markers in peripheral blood (PB) CD4 T cells in a separate cohort of similarly aged persons. Results Frequencies of colonic CD4 T cells as a fraction of total LP mononuclear cells were higher in older persons whereas absolute numbers of colonic LP CD4 T cells per gram of tissue were similar in both age groups. LP CD4 T cells from older versus younger persons exhibited reduced CTLA-4, PD-1 and Ki67 expression. Levels of Bcl-2, CD57, CD25 and percentages of activated CD38+HLA-DR+ CD4 T cells were similar in both age groups. In memory PB CD4 T cells, older age was only associated with increased CD57 expression. Significant age effects for LP CD8 T cells were only observed for CTLA-4 expression, with lower levels of expression observed on cells from older adults. Conclusions Greater age was associated with reduced expression of the co-inhibitory receptors CTLA-4 and PD-1 on LP CD4 T cells. Colonic LP CD8 T cells from older persons also displayed reduced CTLA-4 expression. These age-associated profiles were not observed in older PB memory CD4 T cells. The decline in co-inhibitory receptor expression on colonic LP T cells may contribute to local and systemic inflammation via a reduced ability to limit ongoing T cell responses to enteric microbial challenge.

538 Harnessing cross-dressing dendritic cells to strengthen anti-tumor immunity

2020 ◽  
Vol 8 (Suppl 3) ◽  
pp. A574-A574
Author(s):  
Ellen Duong ◽  
Timothy Fessenden ◽  
Arjun Bhutkar ◽  
Stefani Spranger
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Cancer Cell ◽  
Tumor Immunity ◽  
T Cell Responses ◽  
T Cell Immunity ◽  
Cell Responses ◽  
Cell Immunity ◽  
Cross Dressing

BackgroundCytotoxic (CD8+) T-cells are required for tumor eradication and durable anti-tumor immunity.1 The induction of tumor-reactive CD8+ T-cells is predominately attributed to a subset of dendritic cells (DC) called Batf3-driven DC1, given their robust ability to cross-present antigens for T-cell priming and their role in effector T-cell recruitment.2–4 Presence of the DC1 signature in tumors correlates with improved survival and response to immunotherapies.5–7 Yet, most tumors with a DC1 infiltrate still progress, suggesting that while DC1 can initiate tumor-reactive CD8+ T-cell responses, they are unable to sustain them. Therefore, there is a critical need to identify and engage additional stimulatory DC subsets to strengthen anti-tumor immunity and boost immunotherapy responses.MethodsTo identify DC subsets that drive poly-functional CD8+ T-cell responses, we compared the DC infiltrate of a spontaneously regressing tumor with a progressing tumor. Multicolor flow immunophenotyping and single-cell RNA-sequencing were used to profile the DC compartment of both tumors. IFNγ-ELISpot was performed on splenocytes to assess for systemic tumor-reactive T-cell responses. Sorted DC subsets from tumors were co-cultured with TCR-transgenic T-cells ex vivo to evaluate their stimulatory capacity. Cross-dressing (in vivo/ex vivo) was assayed by staining for transfer of tumor-derived H-2b MHC complexes to Balb/c DC, which express the H-2d haplotype. Protective systemic immunity was assayed via contralateral flank tumor outgrowth experiments.ResultsRegressor tumors were infiltrated with more cross-presenting DC1 than progressor tumors. However, tumor-reactive CD8+ T-cell responses and tumor control were preserved in Batf3-/- mice lacking DC1, indicating that anti-tumor immune responses could be induced independent of DC1. Through functional assays, we established that anti-tumor immunity against regressor tumors required CD11c+ DC and cGAS/STING-independent type-I-interferon-sensing. Single-cell RNA-sequencing of the immune infiltrate of regressor tumors revealed a novel CD11b+ DC subset expressing an interferon-stimulated gene signature (ISG+ DC). Flow studies demonstrated that ISG+ DC were more enriched in regressor tumors than progressor tumors. We showed that ISG+ DC could activate CD8+ T-cells by cross-dressing with tumor-derived peptide-MHC complexes, thereby bypassing the requirement for cross-presentation to initiate CD8+ T-cell-driven immunity. ISG+ DC highly expressed cytosolic dsRNA sensors (RIG-I/MDA5) and could be therapeutically harnessed by exogenous addition of a dsRNA analog to drive protective CD8+ T-cell responses in DC1-deficient mice.ConclusionsThe DC infiltrate in tumors can dictate the strength of anti-tumor immunity. Harnessing multiple stimulatory DC subsets, such as cross-presenting DC1 and cross-dressing ISG+ DC, provides a therapeutic opportunity to enhance anti-tumor immunity and increase immunotherapy responses.ReferencesFridman WH, et al. The immune contexture in human tumours: impact on clinical outcome. Nature Reviews Cancer 2012;12(4): p. 298–306.Hildner K, et al. Batf3 deficiency reveals a critical role for CD8alpha+ dendritic cells in cytotoxic T cell immunity. Science 2008;322(5904):p. 1097–100.Spranger S, et al. Tumor-Residing Batf3 dendritic cells are required for effector T cell trafficking and adoptive T cell therapy. Cancer Cell 2017;31(5):p. 711–723.e4.Roberts, EW, et al., Critical role for CD103(+)/CD141(+) dendritic cells bearing CCR7 for tumor antigen trafficking and priming of T cell immunity in melanoma. Cancer Cell 2016;30(2): p. 324–336.Broz ML, et al. Dissecting the tumor myeloid compartment reveals rare activating antigen-presenting cells critical for T cell immunity. Cancer Cell 2014;26(5): p. 638–52.Salmon H., et al., Expansion and activation of CD103(+) dendritic cell progenitors at the tumor site enhances tumor responses to therapeutic PD-L1 and BRAF inhibition. Immunity, 2016. 44(4): p. 924–38.Sánchez-Paulete AR, et al., Cancer immunotherapy with immunomodulatory anti-CD137 and Anti-PD-1 monoclonal antibodies requires BATF3-dependent dendritic cells. Cancer Discov, 2016;6(1):p. 71–9.

scholarly journals T Cell Immunity against Influenza: The Long Way from Animal Models Towards a Real-Life Universal Flu Vaccine

Viruses ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 199
Author(s):  
Anna Schmidt ◽  
Dennis Lapuente
Keyword(s):  
T Cells ◽  
T Cell ◽  
Animal Models ◽  
Respiratory Tract ◽  
Memory T Cells ◽  
Real Life ◽  
T Cell Immunity ◽  
Cell Immunity ◽  
Flu Vaccine ◽  
Resident Memory T Cells

Current flu vaccines rely on the induction of strain-specific neutralizing antibodies, which leaves the population vulnerable to drifted seasonal or newly emerged pandemic strains. Therefore, universal flu vaccine approaches that induce broad immunity against conserved parts of influenza have top priority in research. Cross-reactive T cell responses, especially tissue-resident memory T cells in the respiratory tract, provide efficient heterologous immunity, and must therefore be a key component of universal flu vaccines. Here, we review recent findings about T cell-based flu immunity, with an emphasis on tissue-resident memory T cells in the respiratory tract of humans and different animal models. Furthermore, we provide an update on preclinical and clinical studies evaluating T cell-evoking flu vaccines, and discuss the implementation of T cell immunity in real-life vaccine policies.

scholarly journals Indoleamine 2,3-dioxygenase specific, cytotoxic T cells as immune regulators

Blood ◽  
2011 ◽  
Vol 117 (7) ◽  
pp. 2200-2210 ◽  
Author(s):  
Rikke Bæk Sørensen ◽  
Sine Reker Hadrup ◽  
Inge Marie Svane ◽  
Mads Christian Hjortsø ◽  
Per thor Straten ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Effector T Cells ◽  
T Cell Immunity ◽  
Regulatory Function ◽  
Cytotoxic T Cell ◽  
Interleukin 17 ◽  
Patients With Cancer ◽  
Indoleamine 2,3 Dioxygenase ◽  
Cell Immunity

Abstract Indoleamine 2,3-dioxygenase (IDO) is an immunoregulatory enzyme that is implicated in suppressing T-cell immunity in normal and pathologic settings. Here, we describe that spontaneous cytotoxic T-cell reactivity against IDO exists not only in patients with cancer but also in healthy persons. We show that the presence of such IDO-specific CD8+ T cells boosted T-cell immunity against viral or tumor-associated antigens by eliminating IDO+ suppressive cells. This had profound effects on the balance between interleukin-17 (IL-17)–producing CD4+ T cells and regulatory T cells. Furthermore, this caused an increase in the production of the proinflammatory cytokines IL-6 and tumor necrosis factor-α while decreasing the IL-10 production. Finally, the addition of IDO-inducing agents (ie, the TLR9 ligand cytosine-phosphate-guanosine, soluble cytotoxic T lymphocyte–associated antigen 4, or interferon γ) induced IDO-specific T cells among peripheral blood mononuclear cells from patients with cancer as well as healthy donors. In the clinical setting, IDO may serve as an important and widely applicable target for immunotherapeutic strategies in which IDO plays a significant regulatory role. We describe for the first time effector T cells with a general regulatory function that may play a vital role for the mounting or maintaining of an effective adaptive immune response. We suggest terming such effector T cells “supporter T cells.”

scholarly journals Glycolysis fuels phosphoinositide 3-kinase signaling to bolster T cell immunity

Science ◽  
2021 ◽  
Vol 371 (6527) ◽  
pp. 405-410
Author(s):  
Ke Xu ◽  
Na Yin ◽  
Min Peng ◽  
Efstathios G. Stamatiades ◽  
Amy Shyu ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Glycolytic Enzyme ◽  
T Cell Immunity ◽  
Pi3k Signaling ◽  
Growth Factor Signaling ◽  
Atp Production ◽  
T Effector Cells ◽  
Cell Immunity ◽  
Phosphoinositide 3 Kinase

Infection triggers expansion and effector differentiation of T cells specific for microbial antigens in association with metabolic reprograming. We found that the glycolytic enzyme lactate dehydrogenase A (LDHA) is induced in CD8+ T effector cells through phosphoinositide 3-kinase (PI3K) signaling. In turn, ablation of LDHA inhibits PI3K-dependent phosphorylation of Akt and its transcription factor target Foxo1, causing defective antimicrobial immunity. LDHA deficiency cripples cellular redox control and diminishes adenosine triphosphate (ATP) production in effector T cells, resulting in attenuated PI3K signaling. Thus, nutrient metabolism and growth factor signaling are highly integrated processes, with glycolytic ATP serving as a rheostat to gauge PI3K-Akt-Foxo1 signaling in the control of T cell immunity. Such a bioenergetic mechanism for the regulation of signaling may explain the Warburg effect.

scholarly journals Limited Foxp3+ Regulatory T Cells Response During Acute Trypanosoma cruzi Infection Is Required to Allow the Emergence of Robust Parasite-Specific CD8+ T Cell Immunity

2018 ◽  
Vol 9 ◽  
Author(s):  
Cintia L. Araujo Furlan ◽  
Jimena Tosello Boari ◽  
Constanza Rodriguez ◽  
Fernando P. Canale ◽  
Facundo Fiocca Vernengo ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Regulatory T Cells ◽  
Trypanosoma Cruzi ◽  
Cd8 T Cell ◽  
T Cell Immunity ◽  
Cell Immunity ◽  
Cruzi Infection
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