Analysis of T-cell cultures and clones from a patient with classic rheumatoid arthritis ? evidence for the existence of autoreactive T-cell clones in blood and synovial fluid

1984 ◽  
Vol 4 (S1) ◽  
pp. 1-9 ◽  
Author(s):  
M. Schlesier ◽  
C. Ramb-Lindhauer ◽  
M. G�rtner ◽  
H. H. Peter
Keyword(s):  
Rheumatoid Arthritis ◽  
T Cell ◽  
Synovial Fluid ◽  
Cell Cultures ◽  
T Cell Clones ◽  
Autoreactive T Cell ◽  
Cell Clones ◽  
Classic Rheumatoid Arthritis

Diversity in antigen recognition byMycobacterium tuberculosis-reactive T cell clones from the synovial fluid of rheumatoid arthritis patients

1991 ◽  
Vol 21 (5) ◽  
pp. 1297-1302 ◽  
Author(s):  
Pieter C. M. Res ◽  
Daniela L. M. Orsini ◽  
Jacob M. van Laar ◽  
Anneke A. M. Janson ◽  
Christiane Abou-Zeid ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
T Cell ◽  
Synovial Fluid ◽  
Antigen Recognition ◽  
T Cell Clones ◽  
Cell Clones

scholarly journals Isolation ofYERSINIA-Specific T Cell Clones from the Synovial Membrane and Synovial Fluid of a Patient with Reactive Arthritis

1991 ◽  
Vol 34 (9) ◽  
pp. 1151-1157 ◽  
Author(s):  
N. J. Viner ◽  
L. C. Bailey ◽  
P. F. Life ◽  
P. A. Bacon ◽  
J. S. H. Gaston
Keyword(s):  
T Cell ◽  
Synovial Fluid ◽  
Reactive Arthritis ◽  
Synovial Membrane ◽  
T Cell Clones ◽  
Cell Clones

scholarly journals Complementary mutations in an antigenic peptide allow for crossreactivity of autoreactive T-cell clones

1996 ◽  
Vol 93 (26) ◽  
pp. 15317-15322 ◽  
Author(s):  
L. J. Ausubel ◽  
C. K. Kwan ◽  
A. Sette ◽  
V. Kuchroo ◽  
D. A. Hafler
Keyword(s):  
T Cell ◽  
Antigenic Peptide ◽  
T Cell Clones ◽  
Autoreactive T Cell ◽  
Cell Clones

Characterisation of cellular and humoral autoimmune responses to histone H1 and core histones in human systemic lupus erythaematosus

2008 ◽  
Vol 68 (1) ◽  
pp. 110-116 ◽  
Author(s):  
G H Stummvoll ◽  
R D Fritsch ◽  
B Meyer ◽  
E Hoefler ◽  
M Aringer ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Cultures ◽  
Mononuclear Cells ◽  
Histone H1 ◽  
Healthy Controls ◽  
Systemic Lupus ◽  
Autoantibody Production ◽  
T Cell Clones ◽  
Cell Clones ◽  
Core Histones

Objective:To address key aspects of anti-histone autoimmunity in systemic lupus erythaematosus (SLE), we performed a detailed characterisation of cellular and humoral autoreactivity to histone H1 and the four core histones H2A, H2B, H3, H4 in patients with SLE and healthy controls.Methods:Peripheral blood mononuclear cells of 41 patients with SLE and 28 healthy controls were exposed to individual histones and proliferation was measured by [3H]-thymidine incorporation. H1-reactive T cell clones were obtained by limiting dilution. Cytokines and total IgG in culture supernatants was measured by ELISA, and autoantibodies to histones were determined by ELISA and immunoblotting.Results:Proliferative responses to H1 were more frequent and more pronounced in cell cultures from patients with SLE (p<0.002), while among the core histones only the response to H2A was increased in patient cultures (p<0.01). All histones elicited a Th1-like cytokine response in patients and controls (high interferon (IFN)γ and tumour necrosis factor (TNF)α, no interleukin (IL)4) with H1 inducing the highest levels of TNFα. However, H1 stimulated production of IgG and anti-histone antibodies only in cell cultures derived from patients with SLE. H1-specific T cell clones from patients and controls showed a CD4+CD28+ phenotype and a Th1 cytokine profile. Anti-histone antibodies were detected in 51% of patients with SLE, were primarily directed to H1, H3 and H4, and predominantly of the IgG2 subtype.Conclusions:Histone H1 constitutes a major B cell and T cell autoantigen in SLE, triggering a proinflammatory Th1 response and driving autoantibody production. This suggests that histone H1 may be of considerable relevance for the pathogenesis of SLE.

Functional evidence for the recognition of endogenous peptides by autoreactive T cell clones

1989 ◽  
Vol 1 (6) ◽  
pp. 624-630 ◽  
Author(s):  
Ann D. M. Rees ◽  
Giovanna Lombardl ◽  
Anne Scoging ◽  
Linda Barber ◽  
David Mitchell ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Clones ◽  
Endogenous Peptides ◽  
Autoreactive T Cell ◽  
Cell Clones

Activation of Autoreactive T-cell clones from NZB.H-2bm12 mice

1994 ◽  
Vol 7 (3) ◽  
pp. 275-290 ◽  
Author(s):  
Mitsuru Naiki ◽  
Steven H. Yoshida ◽  
Aftab A. Ansari ◽  
Jerry Bill ◽  
M.Eric Gershwin
Keyword(s):  
T Cell ◽  
T Cell Clones ◽  
Autoreactive T Cell ◽  
Cell Clones

Abnormal T-cell repertoire is consistent with immune process underlying the pathogenesis of paroxysmal nocturnal hemoglobinuria

Blood ◽  
2000 ◽  
Vol 96 (7) ◽  
pp. 2613-2620
Author(s):  
Anastasios Karadimitris ◽  
John S. Manavalan ◽  
Howard T. Thaler ◽  
Rosario Notaro ◽  
David J. Araten ◽  
...  
Keyword(s):  
T Cell ◽  
Messenger Rna ◽  
Paroxysmal Nocturnal Hemoglobinuria ◽  
Bone Marrow Failure ◽  
Size Analysis ◽  
Cell Repertoire ◽  
Hematopoietic Stem ◽  
T Cell Clones ◽  
Autoreactive T Cell ◽  
Cell Clones

Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired clonal disorder of the hematopoietic stem cell (HSC). Somatic mutations in thePIG-A gene result in the deficiency of several glycosylphosphatidylinositol-linked proteins from the surface of blood cells. This explains intravascular hemolysis but does not explain the mechanism of bone marrow failure that is almost invariably seen in PNH. In view of the close relationship between PNH and idiopathic aplastic anemia (IAA), it has been suggested that the 2 disorders might have a similar cellular pathogenesis, namely, that autoreactive T-cell clones are targeting HSCs. In this paper, we searched for abnormally expanded T-cell clones by size analysis of the complementarity-determining region 3 (CDR3) in the beta variable chain (BV) messenger RNA (mRNA) of the T-cell receptor (TCR) in 19 patients with PNH, in 7 multitransfused patients with hemoglobinopathy. and in 11 age-matched healthy individuals. We found a significantly higher degree of skewness in the TCR BV repertoire of patients with PNH, compared with controls (R2 values 0.82 vs 0.91,P < .001). The mean frequency of skewed families per individual was increased by more than 2-fold in patients with PNH, compared with controls (28% ± 19.6% vs 11.4% ± 6%,P = .002). In addition, several TCR BV families were significantly more frequently skewed in patients with PNH than in controls. These findings provide experimental support for the concept that PNH, like IAA, has an immune pathogenesis. In addition, the identification of expanded T-cell clones by CDR3 size analysis will help to investigate the effect of HSC-specific T cells on normal and PNH HSCs.

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