scholarly journals Regulatory T cells suppress virus-specific antibody responses to Friend retrovirus infection

PLoS ONE ◽  
2018 ◽  
Vol 13 (4) ◽  
pp. e0195402 ◽  
Author(s):  
Tyler C. Moore ◽  
Ronald J. Messer ◽  
Kim J. Hasenkrug
2014 ◽  
Vol 29 (1) ◽  
pp. 48-60 ◽  
Author(s):  
Jara J. Joedicke ◽  
Kirsten K. Dietze ◽  
Gennadiy Zelinskyy ◽  
Ulf Dittmer

2020 ◽  
Vol 33 (5) ◽  
pp. 353-360
Author(s):  
Jean Alexander Ross ◽  
Anna Malyshkina ◽  
Lucas Otto ◽  
Jia Liu ◽  
Ulf Dittmer

2006 ◽  
Vol 74 (6) ◽  
pp. 3519-3529 ◽  
Author(s):  
Maria Kaparakis ◽  
Karen L. Laurie ◽  
Odilia Wijburg ◽  
John Pedersen ◽  
Martin Pearse ◽  
...  

ABSTRACT Gastric Helicobacter spp. induce chronic gastritis that may lead to ulceration and dysplasia. The host elicits a T helper 1 (Th1) response that is fundamental to the pathogenesis of these bacteria. We analyzed immune responses in Helicobacter-infected, normal mice depleted of CD4+ CD25+ T cells to investigate the in vivo role of regulatory T cells (Tregs) in the modulation of Helicobacter immunopathology. BALB/c and transgenic mice were depleted of CD4+ CD25+ T cells by administration of an anti-CD25 antibody either at the time of infection with Helicobacter or during chronic infection and gastritis. Depletion of CD25+ Tregs prior to and during infection of mice with Helicobacter spp. did not affect either bacterial colonization or severity of gastritis. Depletion of CD25+ Tregs was associated with increased Helicobacter-specific antibody levels and an altered isotype distribution. Paragastric lymph node cells from CD25+ Treg-depleted and control infected mice showed similar proliferation to Helicobacter antigens, but only cells from anti-CD25-treated animals secreted Th2 cytokines. CD25+ Tregs do not control the level of gastritis induced by gastric Helicobacter spp. in normal, thymus-intact BALB/c mice. However, CD25+ Tregs influence the cytokine and antibody responses induced by infection. Autoimmune gastritis is not induced in Helicobacter-infected mice depleted of CD25+ Tregs but is induced in CD25+ Treg-depleted mice, which have a higher frequency of autoreactive T cells.


Allergy ◽  
2020 ◽  
Author(s):  
Feng Wang ◽  
Yin Yao ◽  
Hongyan Hou ◽  
Shiji Wu ◽  
Cuilian Guo ◽  
...  

1985 ◽  
Vol 231 (6) ◽  
pp. 307-312 ◽  
Author(s):  
B. Vandvik ◽  
B. Sk�ldenberg ◽  
M. Forsgren ◽  
G. Stiernstedt ◽  
S. Jeansson ◽  
...  

2014 ◽  
Vol 209 (9) ◽  
pp. 1354-1361 ◽  
Author(s):  
Kuan-Ying Arthur Huang ◽  
Chris Ka-Fai Li ◽  
Elizabeth Clutterbuck ◽  
Cecilia Chui ◽  
Tom Wilkinson ◽  
...  

1992 ◽  
Vol 175 (1) ◽  
pp. 211-216 ◽  
Author(s):  
T G Yin ◽  
P Schendel ◽  
Y C Yang

The availability of large quantities of highly purified recombinant interleukin 11 (rhuIL-11) has allowed us to investigate the effects of rhuIL-11 on sheep red blood cell (SRBC)-specific antibody responses in the murine system. The results showed that rhuIL-11 was effective in enhancing the generation of mouse spleen SRBC-specific plaque-forming cells (PFC) in the in vitro cell culture system in a dose-dependent manner. These effects of rhuIL-11 were abrogated completely by the addition of anti-rhuIL-11 antibody, but not by the addition of preimmunized rabbit serum. Cell-depletion studies revealed that L3T4 (CD4)+ T cells, but not Lyt-2 (CD8)+ T cells, are required in the rhuIL-11-stimulated augmentation of SRBC-specific antibody responses. The effects of rhuIL-11 on the SRBC-specific antibody responses in vivo were also examined. RhuIL-11 administration to normal C3H/HeJ mice resulted in a dose-dependent increase in the number of spleen SRBC-specific PFC as well as serum SRBC-specific antibody titer in both the primary and secondary immune responses. In mice immunosuppressed by cyclophosphamide treatment, rhuIL-11 administration significantly augmented the number of spleen SRBC-specific PFC as well as serum SRBC-specific antibody titer when compared with the cyclophosphamide-treated mice without IL-11 treatment. These results demonstrated that IL-11 is a novel cytokine involved in modulating antigen-specific antibody responses in vitro as well as in vivo.


1997 ◽  
Vol 185 (3) ◽  
pp. 551-562 ◽  
Author(s):  
Sanjiv A. Luther ◽  
Adam Gulbranson-Judge ◽  
Hans Acha-Orbea ◽  
Ian C.M. MacLennan

Mouse mammary tumor virus (MMTV[SW]) encodes a superantigen expressed by infected B cells. It evokes an antibody response specific for viral envelope protein, indicating selective activation of antigen-specific B cells. The response to MMTV(SW) in draining lymph nodes was compared with the response to haptenated chicken gamma globulin (NP-CGG) using flow cytometry and immunohistology. T cell priming occurs in both responses, with T cells proliferating in association with interdigitating dendritic cells in the T zone. T cell proliferation continues in the presence of B cells in the outer T zone, and B blasts then undergo exponential growth and differentiation into plasma cells in the medullary cords. Germinal centers develop in both responses, but those induced by MMTV(SW) appear later and are smaller. Most T cells activated in the T zone and germinal centers in the MMTV(SW) response are superantigen specific and these persist for weeks in lymph nodes draining the site MMTV(SW) injection; this contrasts with the selective loss of superantigen-specific T cells from other secondary lymphoid tissues. The results indicate that this viral superantigen, when expressed by professional antigen-presenting cells, drives extrafollicular and follicular B cell differentiation leading to virus-specific antibody production.


2014 ◽  
Vol 88 (9) ◽  
pp. 5200-5201 ◽  
Author(s):  
J. J. Joedicke ◽  
G. Zelinskyy ◽  
U. Dittmer ◽  
K. J. Hasenkrug

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