Amelioration of arthritis through mobilization of peptide-specific CD8+ regulatory T cells

Leavenworth, Jianmei W.; Tang, Xiaolei; Kim, Hye-Jung; Wang, Xiaoyang; Cantor, Harvey

doi:10.1172/jci66938

Cited by 74 publications

(68 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, we did not detect IL-17 (data not shown), a cytokine that has been implicated in pathogenic GC formation in some circumstances (31). jci.org Volume 124 Number 10 October 2014 CD44 hi , CD122, and Ly49 that have been shown to repress spontaneous development of Tfh cells by inducing their apoptotic death, thereby efficiently contributing to the control of autoimmune diseases in both mice and humans (20,21,37). While Figure 4B).…”

Section: Tgf-β Signaling In T Cells Prevents Aberrant Accumulation Ofmentioning

confidence: 89%

“…CD8 + T regulatory cells (CD8 + Tregs) have been reported to prevent the unrestrained development of Tfh cells by inducing their apoptosis after interaction with Qa-1/ peptide complex on the surface of Tfh cells, in a TCR-dependent manner (19,20). Impairing the regulatory activity of CD8 + Tregs results in autoimmunity (20), while adoptive transfer of CD8 + Tregs is sufficient to reduce the number of Tfh cells and blunt the development of rheumatoid arthritis in mice (21), underlining the physiological relevance of CD8 + Treg-mediated control of Tfh cells. These regulatory cells represent 3% to 5% of peripheral CD8 + T cells, are thought to develop in the thymus (19,22), and are characterized by the surface expression of CD44, CD122, and Ly49.…”

Section: Cd4mentioning

confidence: 99%

See 1 more Smart Citation

TGF-β prevents T follicular helper cell accumulation and B cell autoreactivity

McCarron¹,

Marie²

2014

J. Clin. Invest.

101

View full text Add to dashboard Cite

Section: Tgf-β Signaling In T Cells Prevents Aberrant Accumulation Ofmentioning

confidence: 89%

Section: Cd4mentioning

confidence: 99%

TGF-β prevents T follicular helper cell accumulation and B cell autoreactivity

McCarron¹,

Marie²

2014

J. Clin. Invest.

101

View full text Add to dashboard Cite

“…Qa‐1 is expressed at high levels on GC CXCR5 + CD4 + cells, while CXCR5 − CD4 + T cells express very low levels of Qa‐1; hence, Qa‐1‐restricted CXCR5 + CD8 + T cells specifically target CXCR5 + Tfh cells 254. By mediating perforin‐dependent lysis of GC Tfh cells, they reduce the GC response and help to prevent autoantibody development 252, 254, 255. Although Qa‐1‐restricted CD8 + Treg cells express CXCR5, they do not express ICOS or PD‐1 or markers characteristic of CD4 + Treg cells such as FoxP3.…”

Section: Regulatory Cell Populations and Their Relationship To Bnab Imentioning

confidence: 99%

Immunologic characteristics of HIV‐infected individuals who make broadly neutralizing antibodies

Borrow

Moody

2017

Immunological Reviews

View full text Add to dashboard Cite

SummaryInduction of broadly neutralizing antibodies (bnAbs) capable of inhibiting infection with diverse variants of human immunodeficiency virus type 1 (HIV‐1) is a key, as‐yet‐unachieved goal of prophylactic HIV‐1 vaccine strategies. However, some HIV‐infected individuals develop bnAbs after approximately 2‐4 years of infection, enabling analysis of features of these antibodies and the immunological environment that enables their induction. Distinct subsets of CD4+ T cells play opposing roles in the regulation of humoral responses: T follicular helper (Tfh) cells support germinal center formation and provide help for affinity maturation and the development of memory B cells and plasma cells, while regulatory CD4+ (Treg) cells including T follicular regulatory (Tfr) cells inhibit the germinal center reaction to limit autoantibody production. BnAbs exhibit high somatic mutation frequencies, long third heavy‐chain complementarity determining regions, and/or autoreactivity, suggesting that bnAb generation is likely to be highly dependent on the activity of CD4+ Tfh cells, and may be constrained by host tolerance controls. This review discusses what is known about the immunological environment during HIV‐1 infection, in particular alterations in CD4+ Tfh, Treg, and Tfr populations and autoantibody generation, and how this is related to bnAb development, and considers the implications for HIV‐1 vaccine design.

show abstract

“…CD8 Treg-mediated suppression affects T follicular helper cell expansion, enhances antitumor immunity, and curbs antiviral immune responses (16,17). Adoptively transferred CD8 Tregs suppress collagen-induced arthritis and attenuate graft-versus-host disease (18,19). The therapeutic exploitation of phenotypically and functionally diverse human CD8 Tregs has been hampered by insufficient knowledge of their mechanism of action (6,20,21).…”

Section: Introductionmentioning

confidence: 99%