scholarly journals The T helper cell response in Lyme arthritis: differential recognition of Borrelia burgdorferi outer surface protein A in patients with treatment-resistant or treatment-responsive Lyme arthritis.

1994 ◽  
Vol 180 (6) ◽  
pp. 2069-2078 ◽  
Author(s):  
B Lengl-Janssen ◽  
A F Strauss ◽  
A C Steere ◽  
T Kamradt
Keyword(s):  
T Cell ◽  
Borrelia Burgdorferi ◽  
Cell Lines ◽  
Outer Surface ◽  
Cell Response ◽  
T Cell Response ◽  
Surface Proteins ◽  
Lyme Arthritis ◽  
Treatment Resistant ◽  
T Cell Lines

The host response to Borrelia burgdorferi is likely to play a role in the pathogenesis of Lyme arthritis. Whereas most patients with Lyme arthritis can be cured with antibiotic therapy, approximately 10% of the patients have persistent arthritis for months or even several years after antibiotic treatment. In this study, we tested the hypothesis that the T cell response to one or more antigens of B. burgdorferi is different in patients with treatment-responsive or treatment-resistant Lyme arthritis. For this purpose, 313 B. burgdorferi-specific T cell lines were derived from the synovial fluid or peripheral blood of four patients with treatment-responsive Lyme arthritis and five patients with treatment-resistant arthritis. 87 T cell lines from treatment-responsive Lyme arthritis and 112 lines from the treatment-resistant group were examined for the recognition of five recombinant. B. burgdorferi proteins: outer surface proteins A (OspA), B, C, p39, and p93. In both groups of patients, the T cell lines frequently recognized OspB, and only occasionally recognized OspC, p39, and p93. In contrast, OspA was preferentially recognized by T cell lines from patients with treatment-resistant arthritis, but only rarely recognized by T cell lines from patients with treatment-responsive arthritis (odds ratio 28.4, 95% confidence interval 9.2-87.8, p < 0.005). These results are compatible with the hypothesis that the T cell response to B. burgdorferi OspA is involved in the pathogenesis of treatment-resistant Lyme arthritis.

scholarly journals Borrelia burgdorferi activates a T helper type 1-like T cell subset in Lyme arthritis.

1991 ◽  
Vol 174 (3) ◽  
pp. 593-601 ◽  
Author(s):  
H Yssel ◽  
M C Shanafelt ◽  
C Soderberg ◽  
P V Schneider ◽  
J Anzola ◽  
...  
Keyword(s):  
T Cell ◽  
Borrelia Burgdorferi ◽  
Cell Subset ◽  
Chronic Inflammatory Disease ◽  
T Cell Response ◽  
Lyme Arthritis ◽  
T Helper ◽  
Cell Clones ◽  
T Cell Lines

18 cloned T cell lines reactive with Borrelia burgdorferi proteins, all CD3+4+8-TCR-alpha/beta+ and restricted by HLA class II proteins, were isolated from four patients with chronic Lyme arthritis. Analysis of these T cell clones indicated that the T cell response to the Lyme disease spirochete is not oligoclonally restricted; yet all produced the same pattern of lymphokines, resembling that of murine type 1 T helper cells, after antigen-specific or nonspecific stimulation. Therefore, a subset of human CD4+ T cells, with a distinct profile of lymphokine secretion, is selectively activated by the pathogen inciting this chronic inflammatory disease.

Suppression of autoreactive T-cell response to glycoprotein IIb/IIIa by blockade of CD40/CD154 interaction: implications for treatment of immune thrombocytopenic purpura

Blood ◽  
2003 ◽  
Vol 101 (2) ◽  
pp. 621-623 ◽  
Author(s):  
Masataka Kuwana ◽  
Yutaka Kawakami ◽  
Yasuo Ikeda
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Lines ◽  
Antibody Production ◽  
Immune Thrombocytopenic Purpura ◽  
Cell Response ◽  
T Cell Response ◽  
Thrombocytopenic Purpura ◽  
Autoreactive T Cell ◽  
T Cell Lines

The potential immunosuppressive effect of an anti-CD154 monoclonal antibody (mAb) on the pathogenic autoreactive T-cell response was evaluated using an in vitro culture system with glycoprotein IIb/IIIa (GPIIb/IIIa)–reactive T cells from patients with immune thrombocytopenic purpura (ITP). The anti-CD154 mAb did not inhibit T-cell proliferation, but suppressed anti-GPIIb/IIIa antibody production, in bulk peripheral blood mononuclear cell cultures stimulated with GPIIb/IIIa. Repeated antigenic stimulation of GPIIb/IIIa-reactive CD4+ T-cell lines in the presence of anti-CD154 mAb resulted in the loss of proliferative capacity and helper function for promoting anti-GPIIb/IIIa antibody production. These anergic T-cell lines showed a cytokine profile of low interferon γ and high interleukin 10 and suppressed anti-GPIIb/IIIa antibody production. Our results indicate that blockade of the CD40/CD154 interaction induces generation of autoantigen-specific anergic CD4+ T cells with regulatory function and could be a therapeutic option for suppressing pathogenic autoimmune responses in patients with ITP.

scholarly journals Mycobacterium tuberculosis-specific CD4+and CD8+T cells differ in their capacity to recognize infected macrophages

2018 ◽  
Author(s):  
Jason Yang ◽  
Daniel Mott ◽  
Rujapak Sutiwisesak ◽  
Yu Jung Lu ◽  
Fiona Raso ◽  
...  
Keyword(s):  
T Cells ◽  
Mycobacterium Tuberculosis ◽  
T Cell ◽  
Cell Lines ◽  
Cell Response ◽  
Vaccine Development ◽  
T Cell Response ◽  
Small Contribution ◽  
T Cell Lines

AbstractContainment ofMycobacterium tuberculosis(Mtb) infection requires T cell recognition of infected macrophages. Mtb has evolved to tolerate, evade, and subvert host immunity. Despite a vigorous and sustained CD8+T cell response during Mtb infection, CD8+T cells make limited contribution to protection. Here, we ask whether the ability of Mtb-specific T cells to restrict Mtb growth is related to their capacity to recognize Mtb-infected macrophages.We derived CD8+T cell lines that recognized the Mtb immunodominant epitope TB10.44-11and compared them to CD4+T cell lines that recognized Ag85b240-254 or ESAT63-17. While the CD4+T cells recognized Mtb-infected macrophages and inhibited Mtb growth in vitro, the TB10.4-specific CD8+T cells neither recognized Mtb-infected macrophages nor restricted Mtb growth. TB10.4-specific CD8+T cells recognized macrophages infected withListeria monocytogenesexpressing TB10.4. However, over-expression of TB10.4 in Mtb did not confer recognition by TB10.4-specific CD8+T cells. Importantly, CD8+T cells recognized macrophages pulsed with irradiated Mtb, indicating that macrophages can efficiently cross-present the TB10.4 protein and raising the possibility that viable bacilli might suppress cross-presentation. Importantly, polyclonal CD8+T cells specific for Mtb antigens other than TB10.4 recognized Mtb-infected macrophages in a MHC-restricted manner.As TB10.4 elicits a dominant CD8+T cell response that poorly recognizes Mtb-infected macrophages, we propose that TB10.4 acts as a decoy antigen. Moreover, it appears that this response overshadows subdominant CD8+T cell response that can recognize Mtb-infected macrophages. The ability of Mtb to subvert the CD8+T cell response may explain why CD8+T cells make a disproportionately small contribution to host defense compared to CD4+T cells. The selection of Mtb antigens for vaccines has focused on antigens that generate immunodominant responses. We propose that establishing whether vaccine-elicited, Mtb-specific T cells recognize Mtb-infected macrophages could be a useful criterion for preclinical vaccine development.

scholarly journals Immune Response to Individual Maedi-Visna Virus gag Antigens

2006 ◽  
Vol 80 (2) ◽  
pp. 912-919 ◽  
Author(s):  
Inderpal Singh ◽  
Ian McConnell ◽  
Barbara Blacklaws
Keyword(s):  
T Cell ◽  
Cell Lines ◽  
Cell Response ◽  
T Cell Response ◽  
Infected Sheep ◽  
Persistently Infected ◽  
Visna Virus ◽  
Immune Mediated ◽  
Maedi Visna Virus ◽  
T Cell Lines

ABSTRACT The lesions caused by maedi-visna virus (MVV) are known to be immune mediated with a presumed contribution by the response to viral antigens. However, very little is known about the T-cell response to individual viral proteins. We have therefore expressed the three individual gag antigens of MVV strain EV1 (p16, p25, and p14) in a bacterial expression system and used the purified recombinant proteins to analyze the antibody and CD4+ T-cell response to MVV. Plasma samples were taken from sheep after 1 year of infection with MVV. The titers for antibodies in these samples were determined by indirect enzyme-linked immunosorbent assays and were as follows: anti-p25 antibody, 1:400 to >1:3,200; anti-p16 antibody, 1:400 to 1:3,200; and anti-p14 antibody, 1:<100 to 1:3,200. When the induction of antibodies was followed over time postinfection (p.i.), samples positive for anti-p25 were seen by day 24 p.i., followed by anti-p16 by day 45 p.i., and lastly anti-p14 by day 100 p.i. T-cell proliferative responses to all three gag antigens were detected in persistently infected sheep peripheral blood lymphocytes. The antigens were therefore used to raise T-cell lines from persistently infected sheep. These T-cell lines were shown to be specific for the recombinant gag antigens and for viral antigen expressed on infected macrophages. The proliferative response was restricted to major histocompatibility complex class II HLA-DR and so was due to CD4+ T lymphocytes. All three gag antigens may therefore play a role in immune-mediated lesion formation in MVV disease by presentation on infected macrophages in lesions.

scholarly journals Generation of diversity in T cell receptor repertoire specific for pigeon cytochrome c.

1987 ◽  
Vol 165 (2) ◽  
pp. 279-301 ◽  
Author(s):  
S B Sorger ◽  
S M Hedrick ◽  
P J Fink ◽  
M A Bookman ◽  
L A Matis
Keyword(s):  
T Cell ◽  
Cytochrome C ◽  
T Cell Receptor ◽  
Cell Lines ◽  
Dna Sequences ◽  
Cell Receptor ◽  
T Cell Response ◽  
Beta Chain ◽  
Antigen Specificity ◽  
T Cell Lines

17 T cell clones and 3 T cell lines, specific for pigeon cytochrome c, were analyzed for fine specificity and rearranged T cell receptor (TCR) gene elements. Clones of similar fine specificities were grouped into one of four phenotypes, and correlations between phenotype differences and gene usage could be made. All the lines and clones rearranged a member of the V alpha 2B4 gene family to a limited number of J alpha regions. The beta chain was made up of one of three non-cross-hybridizing V beta regions, each rearranging to only one or two J beta s. The use of alternate V beta regions could be correlated with phenotype differences, which were manifested either as MHC- or MHC and antigen-specificity changes. In addition, the presence of alloreactivity, which defined a phenotype difference, could be correlated solely with the use of an alternate J alpha region. These observations were substantiated by prospective analyses of pigeon cytochrome c-specific T cell lines that were selected for alternate MHC specificity or alloreactivity and were found to express the correlated alpha and beta chain rearrangements. Previously, the TCR DNA sequences from two clones, each representing a variant of one phenotype, showed sequence differences only in the N regions of their TCR genes. Since only these two variants, using identical V alpha-J alpha and V beta-J beta gene elements, were repeatedly observed in this study, we would predict that the junctional diversity differences are selectable. In this T cell response, all the gene elements involved in the generation of diversity appear to be selected, and may therefore be important in the determination of TCR specificity. This high degree of receptor gene selection represents a fundamental difference from the diversity seen in several extensively analyzed antibody responses.

Effect of an immunosuppressive factor-derived from choriocarcinoma cell lines on IL-2 dependent T cell response

1989 ◽  
Vol 15 ◽  
pp. 150
Author(s):  
T. Kameda ◽  
N. Matsuzaki ◽  
K. Sawai ◽  
T. Okada ◽  
F. Saji ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Lines ◽  
Cell Response ◽  
T Cell Response ◽  
Immunosuppressive Factor

scholarly journals Prominent T cell response to a selectivelyin vivo expressedBorrelia burgdorferi outer surface protein (pG) in patients with Lyme disease

2001 ◽  
Vol 31 (3) ◽  
pp. 767-776 ◽  
Author(s):  
Yvonne Bauer ◽  
Heidelore Hofmann ◽  
Oliver Jahraus ◽  
Joannis Mytilineos ◽  
Markus M. Simon ◽  
...  
Keyword(s):  
T Cell ◽  
Lyme Disease ◽  
Outer Surface ◽  
Cell Response ◽  
Surface Protein ◽  
T Cell Response ◽  
Outer Surface Protein
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