Follicular Helper T Cells: Lineage and Location

Fazilleau, Nicolas; Mark, Linda; McHeyzer‐Williams, Louise J.; McHeyzer‐Williams, Michael G.

doi:10.1016/j.immuni.2009.03.003

Cited by 525 publications

(519 citation statements)

References 170 publications

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“…4E), we initially surmised that the delay in class-switch may be caused by a defect in CD4 responses. Follicular CD4 T cells in the lymphoid tissues mediate humoral immune response by their interaction with the B cells (Fazilleau et al, 2009;King et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Mouse CMV infection delays antibody class switch upon an unrelated virus challenge

Marandu¹,

Finsterbusch²,

Kröger³

et al. 2014

Experimental Gerontology

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Section: Discussionmentioning

confidence: 99%

Mouse CMV infection delays antibody class switch upon an unrelated virus challenge

Marandu¹,

Finsterbusch²,

Kröger³

et al. 2014

Experimental Gerontology

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“…Furthermore, the RASV-administered MyD88 À/À mice had significantly increased transcriptional levels of bcl-6, IL-21, and CXCR5, but not of T-bet and Gata-3 ( Fig. 3F), suggesting the transcriptional patterns of Tfh cells [21]. Of note, many ICOS 1 cells (stained red) were located inside the B-cell follicles (green) in MyD88 À/À mice after oral RASV challenge (Supporting Information Fig.…”

Section: Expansion Of B-cell Compartment Is Accompanied By Cells and mentioning

confidence: 97%

Expansion of Tfh‐like cells during chronic Salmonella exposure mediates the generation of autoimmune hypergammaglobulinemia in MyD88‐deficient mice

Yang

et al. 2011

Eur J Immunol

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The role of TLR signaling in linking the innate and adaptive immune systems has been a controversial issue that remains to be solved. Here, we determined whether MyD88-dependent TLR signals are required for the generation of B-cell responses during chronic Salmonella infection. Oral administration of recombinant attenuated Salmonella enterica serovar Typhimurium vaccine (RASV) strain in MyD88 À/À mice resulted in chronic infection. Infection was accompanied by enlarged germinal centers and hypergammaglobulinemia with anti-double-stranded DNA (dsDNA)-specific Ab in sera, and the deposition of immune complexes in the kidneys, suggesting onset of autoimmunity. CD4 1 T cells expressing PD-1, CXCR5, ICOS, and IL-21 were dramatically increased in chronically infected mice, indicating the expansion of follicular helper T (Tfh)-like cells. Of note, the depletion of CD4 1 T cells completely blocked the generation of polyclonal IgG Ab in sera after oral RASV challenge. Inflammatory myeloid cells expressing CD11b and Gr-1 accumulated in high numbers in the spleen of MyD88 À/À mice. Interestingly, the blockade of PD-1 or ICOS significantly reduced the hypergammaglobulinemia and dsDNA-specific autoantibody production. Overall, these results suggest that Tfh-like cells in chronic bacterial infection trigger autoimmune hypergammaglobulinemia in a PD-1-and ICOSdependent manner.

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“…IL-21, a member of the common-γ chain family of cytokines, could serve as a rescue mechanism by facilitating crosstalk between CD4+ T cells and CD8+ T cells. Produced primarily by CD4+ T cells, IL-21 is critical for promoting B cell and antibody responses as well as inducing the development of the Th17 and T follicular helper lineages (Fazilleau et al, 2009;Korn et al, 2007;Ozaki et al, 2002). IL-21 specifically maintains CD8+ T cell effector activity through the help of CD4+ T cells during chronic viral infection, as has been observed in lymphocytic choriomeningitis virus infection (Elsaesser et al, 2009).…”

Section: Introductionmentioning

confidence: 93%

HCV-Specific Interleukin-21+CD4+ T Cells Responses Associated with Viral Control through the Modulation of HCV-Specific CD8+ T Cells Function in Chronic Hepatitis C Patients

Feng

Zhang

Zeng

et al. 2013

Molecules and Cells

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Interleukin-21 (IL-21)+CD4+ T cells are involved in the immune response against hepatitis B virus (HBV) by secreting IL-21. However, the role of IL-21+CD4+ T cells in the immune response against chronic hepatitis C (CHC) virus infection is poorly understood. This study aimed to investigate the role of IL-21+CD4+ T cells in CHC patients and the potential mechanisms. The study subjects included nineteen CHC patients who were grouped by viral load (low, < 10 6 RNA copies/ml, n = 8; high, > 10 6 RNA copies/ml, n = 11). The peripheral frequency of HCV-specific IL-21+CD4+ T cells was higher in the low viral load group and was negatively correlated with the serum HCV RNA viral load in all CHC patients. Meanwhile, IL-21+ cells accumulated in the liver in the low viral load group. In vitro, IL-21 treatment increased the expression of proliferation markers and cytolytic molecules on HCV-specific CD8+ T cells. In summary, these findings suggest that HCV-specific IL-21+CD4+ T cells might contribute to HCV control by rescuing HCV-specific CD8+ T cells in CHC patients.

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Follicular Helper T Cells: Lineage and Location

Cited by 525 publications

References 170 publications

Mouse CMV infection delays antibody class switch upon an unrelated virus challenge

Mouse CMV infection delays antibody class switch upon an unrelated virus challenge

Expansion of Tfh‐like cells during chronic Salmonella exposure mediates the generation of autoimmune hypergammaglobulinemia in MyD88‐deficient mice

HCV-Specific Interleukin-21+CD4+ T Cells Responses Associated with Viral Control through the Modulation of HCV-Specific CD8+ T Cells Function in Chronic Hepatitis C Patients

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