scholarly journals THU0039 DECIPHERING DISEASE-RELEVANT T CELL SUBSETS IN RHEUMATOID ARTHRITIS IDENTIFIES A NOVEL CELLULAR SUBSET OF PATHOGENETIC IMPORTANCE IN THERAPEUTIC RESISTANCE.

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 232.1-233
Author(s):  
M. Nyirenda ◽  
I. Mcinnes ◽  
C. Goodyear
Keyword(s):  
Rheumatoid Arthritis ◽  
T Cells ◽  
T Cell ◽  
Inflammatory Cytokines ◽  
Regulatory T Cell ◽  
Cell Subset ◽  
T Cell Subsets ◽  
Healthy Controls ◽  
T Cell Subset ◽  
Pro Inflammatory Cytokines

Background:Aberrant T cell responses are key in driving autoimmunity and are commonly associated with rheumatoid arthritis (RA). Unravelling pathways of importance in therapeutic partial response and failure is of critical importance, as this will potentially provide new insights into key drivers of immune-mediated pathogenesis.Objectives:To delineate disease-relevant T cell subsets in RA and assess their potential to act as cellular markers amenable to precision medicine approaches, particularly in the context of therapeutic partial or non-response.Methods:FACS-based immunophenotyping and ex-vivo functional response profiles of CD4+CD161+CCR2+CCR5+T cells were performed in peripheral blood mononuclear cells (PBMC) obtained from patients with RA and healthy controls, using previously characterised methodologies. RA patients fulfilled the 2010 ACR/EULAR criteria for RA. All samples were obtained after written consent, with the appropriate ethical approvals in place.Results:RA patients harboured a higher frequency of CCR2+CCR5+cells within the CD4+CD161+T cell compartment compared with healthy controls. In RA patients this T cell subset had a higher proportion of cells that secrete pro-inflammatory cytokines such as IL-17A, GM-CSF, IFN-γ, and TNF. Importantly, the CD4+CD161+CCR2+CCR5+T cell subset was significantly increased in DMARD non-responders compared to both responders and healthy controls. Moreover, in DMARD non-responders, these cells had a propensity to express increased proportions of pro-inflammatory cytokines. Notably, there was also a significant increase in the ratio of effector: regulatory T cell (Teff: Treg) compared to both responders and healthy controls. In addition, the CD4+CD161+CCR2+CCR5+T cell subset was less responsive to suppression by Tregs. In further support of a role for this T cell population in disease pathogenesis, the frequency of CD4+CD161+CCR2+CCR5+T cells significantly correlated with disease activity, as measured by the DAS28 (R2= 0.65; p = 0.003; n=11).Conclusion:Combined, our findings suggest that the CD4+CD161+CCR2+CCR5+T cell subset represents a substantially abnormal T cell subset in RA, exhibiting exaggerated pro-inflammatory responses, numerical abundance relative to Tregs, and resistant to regulation by Tregs. The CD4+CD161+CCR2+CCR5+T cell subset appears to be a marker of therapeutic response status in RA, via its contribution to disease pathology and highlights this subset as a potential therapeutic target in RA.References:[1]McInnes IB, Schett G. The pathogenesis of rheumatoid arthritis.N Engl J Med. 2011;365(23):2205-19.[2]Mexhitaj I, Nyirenda MH, Li R, O’Mahony J, Rezk A, Rozenberg A,et al. Abnormal effector and regulatory T cell subsets in paediatric-onset multiple sclerosis.Brain. 2019;142(3):617-32.[3]Cosmi L, Cimaz R, Maggi L, Santarlasci V, Capone M, Borriello F,et al. Evidence of the transient nature of the Th17 phenotype of CD4+CD161+T cells in the synovial fluid of patients with juvenile idiopathic arthritis.Arthritis Rheum. 2011;63(8):2504-15.Disclosure of Interests:Mukanthu Nyirenda: None declared, Iain McInnes Grant/research support from: Bristol-Myers Squibb, Celgene, Eli Lilly and Company, Janssen, and UCB, Consultant of: AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly and Company, Gilead, Janssen, Novartis, Pfizer, and UCB, Carl Goodyear: None declared

scholarly journals In human alloreactive CD4+ T-cells, dichloroacetate inhibits aerobic glycolysis, induces apoptosis and favors differentiation towards the regulatory T-cell subset instead of effector T-cell subsets

2016 ◽  
Vol 13 (4) ◽  
pp. 3370-3376 ◽  
Author(s):  
THEODOROS ELEFTHERIADIS ◽  
MARIA SOUNIDAKI ◽  
GEORGIOS PISSAS ◽  
GEORGIA ANTONIADI ◽  
VASSILIOS LIAKOPOULOS ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Regulatory T Cell ◽  
Cd4 T Cells ◽  
Aerobic Glycolysis ◽  
Cell Subset ◽  
T Cell Subsets ◽  
T Cell Subset ◽  
Effector T Cell

scholarly journals Novel Senescent Regulatory T-Cell Subset with Impaired Suppressive Function in Rheumatoid Arthritis

2017 ◽  
Vol 8 ◽  
Author(s):  
Johannes Fessler ◽  
Andrea Raicht ◽  
Rusmir Husic ◽  
Anja Ficjan ◽  
Christine Schwarz ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
T Cell ◽  
Regulatory T Cell ◽  
Cell Subset ◽  
T Cell Subset ◽  
Suppressive Function

scholarly journals Reconstitution of T Cell Subsets Following Allogeneic Hematopoietic Cell Transplantation

Cancers ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1974 ◽  
Author(s):  
Linde Dekker ◽  
Coco de Koning ◽  
Caroline Lindemans ◽  
Stefan Nierkens
Keyword(s):  
Overall Survival ◽  
T Cells ◽  
T Cell ◽  
Cell Transplantation ◽  
Hematopoietic Cell Transplantation ◽  
Cell Subset ◽  
Γδ T Cells ◽  
Hematopoietic Cell ◽  
T Cell Subsets ◽  
T Cell Subset

Allogeneic (allo) hematopoietic cell transplantation (HCT) is the only curative treatment option for patients suffering from chemotherapy-refractory or relapsed hematological malignancies. The occurrence of morbidity and mortality after allo-HCT is still high. This is partly correlated with the immunological recovery of the T cell subsets, of which the dynamics and relations to complications are still poorly understood. Detailed information on T cell subset recovery is crucial to provide tools for better prediction and modulation of adverse events. Here, we review the current knowledge regarding CD4+ and CD8+ T cells, γδ T cells, iNKT cells, Treg cells, MAIT cells and naive and memory T cell reconstitution, as well as their relations to outcome, considering different cell sources and immunosuppressive therapies. We conclude that the T cell subsets reconstitute in different ways and are associated with distinct adverse and beneficial events; however, adequate reconstitution of all the subsets is associated with better overall survival. Although the exact mechanisms involved in the reconstitution of each T cell subset and their associations with allo-HCT outcome need to be further elucidated, the data and suggestions presented here point towards the development of individualized approaches to improve their reconstitution. This includes the modulation of immunotherapeutic interventions based on more detailed immune monitoring, aiming to improve overall survival changes.

scholarly journals DOP29 Elevation of a novel blood-based gene signature in a severe Crohn’s disease (CD) subtype preceding surgery defines and predicts a post-surgical decrease in pro-inflammatory pathway activation

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S068-S069
Author(s):  
R Gonsky ◽  
P Fleshner ◽  
G Botwin ◽  
E Biener-Ramanujan ◽  
D McGovern ◽  
...  
Keyword(s):  
Gene Expression ◽  
T Cells ◽  
T Cell ◽  
Cell Subset ◽  
Gene Signature ◽  
T Cell Subsets ◽  
T Cell Subset ◽  
Post Surgery ◽  
Cell Gene Expression ◽  
Cell Gene

Abstract Background CD is defined by transmural inflammation leading to inflammatory, stricturing and/or penetrating phenotypes. Identifying underlying molecular pathways and distinct disease subsets is critical for improved prognostics, therapeutics and biomarker discovery. Methods CD3+ T cells were purified from paired blood and mucosal tissue from 101 CD and 17 non-IBD subjects requiring surgery. Longitudinal samples (n = 30) were collected 4–13 mo. post-surgery. Expression profiles were generated by RNAseq, T-cell subset deconvolution by xCell and transcriptome-wide associations (TWAS) using TWAS-hub. Results Unsupervised clustering of peripheral T-cell gene expression at surgery revealed 2 CD profiles: Expression from cluster1, labelled CD-PBT (63%), clustered tightly with the non-IBD group. In cluster2, expression shifted from a peripheral toward a mucosal profile, labelled CD-PBmu(cosal) (37%). CD-PBmu was defined by differentially expressed genes (DEG) (1944 DEG, p < 0.001) regulating cell migration and adhesion pathways and a distinct T-cell subset composition associated with stricturing disease (p = 0.03), increased resected bowel length (p = 0.036) and post-op recurrence (p = 0.01). There were no significant differences in disease location/behaviour. Independent validation (5 public datasets) confirmed the CD-PBmu signature in data from whole blood (CD patients failing anti-TNF therapy, n = 204) and the mucosal-like expression profile in data from ileal tissue (paediatric CD patients, studies n = 751). A defining feature of CD-PBmu, validated in a separate CD cohort (n = 19), was decreased pro-inflammatory cytokine/chemokine and adhesion molecule expression following surgery (900 DEG, p < 0.001). No post-surgery change in expression was detected in CD-PBT. A 44-gene classifier was identified to enable clinical application. The classifier accurately detected the CD-PBmu patient subtype, correlated with the altered composition of peripheral T-cell subsets and overlapped with IBD associated TWAS signals (>60%). Recently, another group posed a blood-based 17 gene panel as predictive for aggressive IBD. These genes were not predictive for either the CD-PBmu or CD-PBT subtype (<50% DEG). Conclusion Severe CD can be stratified into 2 subtypes based on peripheral T-cell gene expression. Circulating T cells from CD-PBmu exhibit a mucosal-like gene signature, altered T-cell subset composition, clinical features of severity and decreased pro-inflammatory gene expression post-surgery. These findings hold potential to identify targets for CD subtype-specific therapeutic development. The 44-gene classifier overlapped with multiple paediatric CD datasets, suggesting the potential application of these findings for treatment stratification early in the disease process.

Imbalance between CD8+CD28+ and CD8+CD28– T-cell subsets and its clinical significance in patients with systemic lupus erythematosus

Lupus ◽  
2019 ◽  
Vol 28 (10) ◽  
pp. 1214-1223
Author(s):  
S Minning ◽  
Y Xiaofan ◽  
X Anqi ◽  
G Bingjie ◽  
S Dinglei ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cells ◽  
T Cell ◽  
Lupus Erythematosus ◽  
Fas Ligand ◽  
Activity Index ◽  
Cell Subset ◽  
T Cell Subsets ◽  
Systemic Lupus ◽  
T Cell Subset

Objective The aim of this study was to evaluate the changes in CD8+CD28–/CD8+CD28+ T-cell subset balance and in the CD8+CD28– Treg cell number and function in patients with systemic lupus erythematosus (SLE). Methods Cell isolation and flow cytometry analysis were employed to investigate the T-cell subsets. Results It was found that in high-activity SLE patients, the CD8+CD28+ T-cell subset was reduced, which was inversely correlated with the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI), and that the CD8+CD28–/CD8+CD28+ ratio was elevated, which was positively correlated with SLEDAI and with renal damage and inversely correlated with serum complement level, whereas the CD8+CD28– T-cell subset was increased only in inactive patients. It was also found that apoptosis of CD8+ T cells increased, and Fas, Fas ligand (FasL) and interleukin (IL)-6 expression were high, whereas cytotoxic T-lymphocyte–associated antigen 4 (CTLA-4) expression was low by the CD8+CD28+ T cell subset in active SLE patients; apoptosis was positively correlated with SLEDAI and with the expression of Fas and FasL by the CD8+CD28+ T-cell subset in active SLE patients. IL-6 and CTLA-4 expression were found to be low by the CD8+CD28– T cell subset in active SLE patients. Conclusion These data suggest that high expression of Fas, FasL and IL-6 and low expression of CTLA-4 by the CD8+CD28+ T-cell subset promotes the activation-induced cell death of the CD8+CD28+ T-cell subset, resulting in an imbalance of CD8+CD28–/CD8+CD28+ T cells in active SLE patients, which represents an important feature in the immunological pathogenesis of SLE. The CD8+CD28– T-cell subset may play some role in inactive SLE.

Mechanisms by Which NK T Cells Become the Predominant T Cell Subset in Mice after Irradiation.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4295-4295
Author(s):  
Zhenyu Yao ◽  
Yinping Liu ◽  
Jennifer McIntire ◽  
Samuel Strober
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Subset ◽  
Absolute Number ◽  
T Cell Subsets ◽  
Brdu Incorporation ◽  
T Cell Subset ◽  
Nk T Cells ◽  
The Absolute ◽  
Nk T Cell

Abstract Previously, we found that the percentage of NK T cells among all T cells in the spleen of mice treated with fractionated irradiation to the lymphoid tissues (Total lymphoid irradiation; TLI) with a total dose of 4,080 cGy increased markedly due to greater reduction in the absolute number of non-NK T cells as compared to NK T cells. The underlying mechanisms of the change in the T cell subsets after irradiation remained to be established. In the current study, C57BL/6 mice were given escalating single doses of 240, 1,000, 2,000 and 3,000 cGy total body irradiation (TBI). Splenocytes were harvested at 4 or 24 hours after irradiation, and the percentage and absolute number of NK T and non-NK T cells was determined. At the same time, the intracellular level of the anti-apoptotic protein, Bcl-2 was assayed by flow cytometry. In some studies, the turnover rate of NK T cells and non-NK T cells was examined by injection of BrdU and intracellular staining. At 4 hours after all doses of irradiation, neither the NK T nor non-NK T cell subset had a significant change in percentage or absolute number as compared to untreated controls. However, at 24 hours the percentage of NK T cells among all T cells had progressively increased with increased doses of TBI from 3% in the untreated controls to 65% in mice given 3,000 cGy. Whereas the absolute number of non-NK T cells decreased at least 1000 fold, the absolute number of NK T cells decreased approximately 50 fold after 3,000 cGy. The BrdU incorporation of NK T cells from irradiated mice was markedly reduced as compared to untreated mice, and was similar to that of non NK T cells in these irradiated mice. 8–12% of NK T cells and non NK T cells in untreated mice expressed a high level Bcl-2. As the dose of TBI increased progressively, the percentage of Bcl-2hi cells increased progressively to 89% amongst NK T cells and 70% amongst non-NK T cells. At each irradiation dose, the percentage of Bcl-2hi cells amongst NK T cells was higher than amongst non-NK T cells. There were 40×103 Bcl-2hi NK T cell and 10×103 Bcl-2hi non-NK T cells surviving per spleen at 24 hours after 3000 cGy TBI. The absolute number of Bcl-2hi NK T cells decreased by about two fold while the absolute number of Bcl-2hi non-NK T cells decreased by about 100 fold. These results indicate that the increased percentage of NK T cells amongst all T cells after irradiation is due to greater radioresistance rather than to more rapid replenishment of NK T cells as compared to non-NK T cells. We are investigating whether Bcl-2 plays a critical role in the extraordinary radioresistance of the NK T cells.

TH17 Pathway and Associated Pro-Inflammatory Cytokines Promote Immune Dysfunction in Myeloma.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3517-3517
Author(s):  
Rao Prabhala ◽  
Dheeraj Pelluru ◽  
Paola Neri ◽  
Mariateresa Fulciniti ◽  
James J. Driscoll ◽  
...  
Keyword(s):  
T Cell ◽  
Immune Function ◽  
Inflammatory Cytokines ◽  
Th17 Cells ◽  
Cell Subset ◽  
Immune Dysfunction ◽  
T Cell Subsets ◽  
Cytokine Network ◽  
High Level ◽  
Pro Inflammatory Cytokines

Abstract Multiple myeloma (MM) is associated with significant immune dysfunction. Although various mechanisms mediating immune dysregulation in MM have been studied, its molecular and cellular basis is ill defined. IL-6, TGF-β and IL-1β have been implicated in this process, but their mechanism of effects on immune function have not been studied in MM. Together, IL-6 and TGF-β enhance the generation of TH17 cells, important in the development of immunity and auto-immunity. Additionally, TH17 cells are differentiated by number of inflammatory cytokines including, IL-21, IL-22, IL-23, and IL-27. Therefore, we evaluated the immune dysfunction and the role of TH17 cells and associated pro-inflammatory cytokines in myeloma. We have previously characterized that the production of TH1 mediated cytokines including IFN-γ following anti-CD3-mediated activation is significantly lower in myeloma PBMC compared to normal PBMC. We hypothesize that this may be regulated via skewing the immune system towards TH17 pathway. We observed that TH17 cells, measured by intra-cellular flow cytometry, are significantly increased in number in myeloma (16.9%) and MGUS (6.2%) compared to normal (3.3%). Furthermore, we analysed supporting pro-inflammatory cytokine network for the generation of TH17 cells in myeloma, which may be responsible for the observed TH17 skewing of T cell subsets. Sera from MGUS (n=12) and myeloma (n=17) patients were evaluated for the presence of these pro-inflammatory cytokines compared with normal sera (n=6) using ELISA. We observed significant increase in serum IL-21, IL-22 and IL-23 in MGUS (373 pg/ml, 14 pg/ml and 147 pg/ml respectively; p<0.05) and myeloma (296 pg/ml, 12 pg/ml and 215 pg/ml respectively; p<0.05) compared with normal (63 pg/ml, 1.5 pg/ml and 39 pg/ml respectively). In addition, we also observed that the myeloma PBMC stimulated in the presence of IL-6 and TGF-β, both of the cytokines present at a high level in myeloma, induced significant IL-23 production compared with normal. Importantly, IL-23 levels were 10 fold higher in myeloma BM samples compared with matching blood samples. These results indicate that the cytokines from myeloma BM microenvironment may be responsible for the observed T cell subset abnormality by favouring TH17 cells via IL-23/IL-21 production. These cytokines thus may be targets to modulate immune responses in myeloma to enhance immune function and devise effective vaccination strategies in the future.

Apoptotic Pathways of Human Regulatory T Cells in Chronic Graft Versus Host Disease (cGVHD) After Allogeneic Hematopoietic Stem Cell Transplantation (HSCT)

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 225-225
Author(s):  
Kazuyuki Murase ◽  
Yutaka Kawano ◽  
Jeremy Ryan ◽  
Ken-ichi Matsuoka ◽  
Gregory Bascug ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd8 T Cells ◽  
Low Dose ◽  
Cell Subset ◽  
Mitochondrial Pathway ◽  
T Cell Subsets ◽  
T Cell Subset ◽  
Mitochondrial Membrane Depolarization

Abstract Abstract 225 CD4+CD25+Foxp3+ regulatory T cells (Treg) are known to play a central role in the maintenance of self-tolerance and immune homeostasis. After allogeneic stem cell transplantation, impaired recovery of Treg is associated with the development of cGVHD. Interleukin-2 (IL-2) is a critical regulator of Treg development, expansion and survival and lack of IL-2 results in Treg deficiency. In patients with cGVHD, we previously demonstrated that Treg proliferate at high levels but this subset is also highly susceptible to apoptosis leading to inadequate Treg numbers (Matsuoka et al. JCI 2010). We also reported that low-dose IL-2 administration resulted in selective expansion of Treg in vivo and clinical improvement of cGVHD (Koreth et al. NEJM 2011). To identify mechanisms responsible for increased Treg susceptibility to apoptosis in cGVHD we used a new flow cytometry-based assay to measure mitochondrial membrane depolarization in response to a panel of pro-apoptotic BH3 peptides (BIM, BID, BAD, NOXA, PUMA, BMF, HRK). This assessment allowed us to compare BH3 peptide-induced mitochondrial membrane depolarization (“priming”) in different T cell subsets, including CD4 Treg, conventional CD4 T cells (CD4 Tcon), and CD8 T cells. Expression of Bcl-2, CD95 and Ki67 were also studied in each T cell subset. We studied peripheral blood samples from 36 patients with hematologic malignancies (median age 59 yr) who are > 2 years post HSCT (27 patients with cGVHD and 9 patients without cGVHD) and 15 patients who received daily subcutaneous IL-2 for 8 weeks for treatment of steroid-refractory cGvHD. Severity of cGVHD was classified according to NIH criteria. In patients without cGVHD, BH3 priming was similar in all 3 T cell subsets (CD4 Treg, CD4 Tcon and CD8). In patients with cGVHD, CD4 Treg were more primed than CD4 Tcon when challenged with BIM, BAD, PUMA, BMF and the combination of BAD + NOXA peptides (p<0.01 – 0.0001). Treg were more primed than CD8 T cells when challenged with PUMA peptide (p<0.0001), but priming in Treg and CD8 T cells was similar for other BH3 peptides in patients with cGVHD. We also compared BH3 priming of each T cell subset in patients with different grades of cGVHD. When challenged with BH3 peptides, Treg, Tcon and CD8 T cells were less primed in patients with severe cGVHD. In patients with cGVHD, Treg expressed higher levels of Ki-67, higher levels of CD95 and lower levels of Bcl-2 than Tcon. Expression of CD95 did not vary with severity of GVHD in any T cell subset, but expression of Bcl-2 was significantly increased in all subsets in patients with severe cGVHD. Increased BH3 priming and high expression of CD95 indicate that Treg are more susceptible to apoptosis than Tcon in cGVHD. However, both Treg and Tcon become less primed and Bcl-2 levels increase in severe cGVHD suggesting that these cells are less susceptible to mitochondrial pathway apoptosis. Since the total number of Treg and Tcon are significantly reduced in patients with cGVHD, these findings suggest that the remaining circulating cells are relatively resistant to mitochondrial pathway apoptosis. CD95 expression in Treg remains high indicating no change in death receptor pathway apoptosis. Daily treatment with low-dose IL-2 for 8 weeks selectively expands Treg in vivo in patients with severe cGVHD. As the number of Treg increase, BH3 profiling shows that these cells gradually become more primed and therefore more susceptible to mitochondrial pathway apoptosis. Taken together, these studies help define the complex and distinct pathways that regulate survival in different T cell subsets and changes in these pathways that occur in patients with chronic GVHD. These pathways play important roles in the maintenance of T cell homeostasis and targeting these complex pathways can provide new opportunities to promote immune tolerance after allogeneic HSCT. Disclosures: No relevant conflicts of interest to declare.

Biology of porcine T lymphocytes

2006 ◽  
Vol 7 (1-2) ◽  
pp. 81-96 ◽  
Author(s):  
Wasin Charerntantanakul ◽  
James A. Roth
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Lymphocytes ◽  
Cell Subset ◽  
Γδ T Cells ◽  
T Cell Responses ◽  
T Cell Subsets ◽  
Γδ T Cell ◽  
T Cell Subset ◽  
Cell Responses

The present review concentrates on the biological aspects of porcine T lymphocytes. Their ontogeny, subpopulations, localization and trafficking, and responses to pathogens are reviewed. The development of porcine T cells begins in the liver during the first trimester of fetal life and continues in the thymus from the second trimester until after birth. Porcine T cells are divided into two lineages, based on their possession of the [@@@]\rmalpha [@@@]β or γδ T-cell receptor. Porcine [@@@]\rmalpha [@@@]β T cells recognize antigens in a major histocompatibility complex (MHC)-restricted manner, whereas the γδ T cells recognize antigens in a MHC non-restricted fashion. The CD4+CD8−and CD4+CD8loT cell subsets of [@@@]\rmalpha [@@@]β T cells recognize antigens presented in MHC class II molecules, while the CD4−CD8+T cell subset recognizes antigens presented in MHC class I molecules. Porcine [@@@]\rmalpha [@@@]β T cells localize mainly in lymphoid tissues, whereas γδ T cells predominate in the blood and intestinal epithelium of pigs. Porcine CD8+[@@@]\rmalpha [@@@]β T cells are a prominent T-cell subset during antiviral responses, while porcine CD4+[@@@]\rmalpha [@@@]β T cell responses predominantly occur in bacterial and parasitic infections. Porcine γδ T cell responses have been reported in only a few infections. Porcine T cell responses are suppressed by some viruses and bacteria. The mechanisms of T cell suppression are not entirely known but reportedly include the killing of T cells, the inhibition of T cell activation and proliferation, the inhibition of antiviral cytokine production, and the induction of immunosuppressive cytokines.

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