Molecular aspects of autoimmunity

Theofilopoulos, Argyrios N.; Kofler, Reinhard

doi:10.1016/0167-5699(89)90318-6

Cited by 11 publications

(2 citation statements)

References 25 publications

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“…Coexpression of CD4 and CD8 has been found on a special subset of activated [5] and autoreactive [37] T cells. CD4-CD8-T cells represent fetal-type lymphocytes that can react extensively with self antigens [32] and are increased in autoimmune diseases [21,43,56] and some granulomatous reactions [36]. They furthermore to a high degree represent the TcR y/5bearing T cells [3,6,10,18,27,32,38].…”

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confidence: 99%

CD4⁺, CD8⁺, and CD4⁻ CD8⁻ T Cells in CSF and Blood of Patients with Multiple Sclerosis and Tension Headache

et al. 1990

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Two-colour flow cytometric analysis was performed on paired samples of peripheral blood (PB) and cerebrospinal fluid (CSF) of patients with untreated multiple sclerosis (MS) and, for reference, subjects with muscular tension headache (TH) using anti-CD3, anti-CD4, anti-CD8, and anti-HLA-DR monoclonal antibodies in different combinations. CD4+/CD8+ T-cell ratio was increased in CSF compared to PB in both MS patients and TH subjects to a similar extent. This was mainly due to higher CD4+ T-cell levels in the CSF compartment. The proportion of HLA-DR+ T cells was higher in CSF than PB in both MS and TH; this increase of DR+ T cells in CSF was more prominent in MS. The level of CD4+ CD8+ T cells, which represent a subset of activated T cells, was not different between CSF and PB, either in MS or in TH. The proportion of CD4- CD8- T cells, which were found generally not to be blast cells, was lower in CSF compared to PB in both patient groups. However, their CSF level was higher and their PB level lower in MS compared to TH. Results point to an accumulation of activated T-helper cells in the CSF of both MS patients and healthy subjects. Fetal-type CD4- CD8- T cells bearing the unusual T-cell receptor gamma/delta seem to be selectively recruited to the CSF of MS patients.

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confidence: 99%

CD4⁺, CD8⁺, and CD4⁻ CD8⁻ T Cells in CSF and Blood of Patients with Multiple Sclerosis and Tension Headache

et al. 1990

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“…We are presently attempting to extend our investigations of this hypothesis by correlating F2 autoimmunity at the IgVH and V, loci. Recent reports of a uniqueV, gene associated with (NZB x NZW)F1 autoimmunity [33], and the fact that both Ig x and TcR p chain loci are located on chromosome 6 in mouse, suggest the complexity of disease acceleration in these mice may extend beyond H-2 and TcR associations.…”

Section: Discussionmentioning

confidence: 98%

Correlations of autoimmunity with H2 and T cell receptor β chain genotypesin (NZB x NZW) F₂ mice

McConahey

Cardenas

1990

Eur J Immunol

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Accelerated autoimmunity as expressed by the classical autoimmune strain mouse (NZB x NZW)F1 is thought to be the result of major histocompatibility complex (MHC)-associated NZW genes acting on a genetic predisposition for autoimmunity as expressed by the NZB mouse. To evaluate more accurately both H-2 and T cell receptor (TcR) beta chain involvement in F1 disease, we studied the segregation of NZB (H-2d, TcRB) and NZW (H-2z, TcRW) haplotypes of these genetic elements and the development of autoimmunity in (NZB x NZW)F2 generation mice. F2 mice with the H-2d/z genotype lived shorter average life-spans and expressed elevated levels of antibodies to gp70, ssDNA and dsDNA, while those with the TcRW/W genotype (homozgous for the NZW TcR deletion) expressed elevated levels of autoantibodies but had relatively long life-spans. On the other hand, mice with the TcRB/B genotype (homozygous for the NZB TcR) produced consistently low levels of autoantibodies but died at an early age. The most severely affected F2 population were the mice carrying both the TcRB/B and H-2d/z alleles. These mice died on an average within the first 5 months of life, but produced the lowest levels of antibodies to gp70, single-stranded DNA and double-stranded DNA. These data confirm the contribution of NZW H-2-linked genes to accelerated autoimmunity in the F1 hybrid and, furthermore, define NZB TcR-linked components as primary developers of this phenomenon. They also suggest a limited, if any, contribution of both the NZW TcR deletion and traditional autoantibodies to F1 accelerated autoimmunity.

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Abnormal behavior of γ‐committed B lymphocytes probed by a lymphocyte blastogenesis inhibitory factor in autoimmune MRL mice

et al. 1990

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Recently, we have characterized a lymphocyte blastogenesis inhibitory factor (LBIF) which was purified from the culture supernatant of a human histiocytic lymphoma U-937 (Sugimura, K. et al., Eur. J. Immunol. 1989. 19: 1357). In this study, we investigated the effect of LBIF on the antibody production of autoimmune MRL mice in vitro. We demonstrated here that (a) LBIF inhibited the IgM, IgG and IgA antibody responses of lipopolysaccharide (LPS)-stimulated spleen cells of normal BALB/c mice, (b) in the case of old autoimmune MRL/Mp-lpr/lpr (MRL/l) and MRL/Mp-(+)/+ mice, however, LBIF inhibited IgM and IgA but not IgG responses of LPS-stimulated spleen cells, (c) the antibody production of all IgG subclasses, IgG3, IgG1, IgG2b and IgG2a, was not sensitive to LBIF inhibitory activity in these autoimmune mice, (d) in young MRL mice (3-5-week-old MRL/l), which were phenotypically normal, LPS-induced antibody production of all isotypes (IgM, IgG and IgA) was strongly inhibited by LBIF as shown in normal BALB/c mice and (e) in the case of 7-week-old MRL/l the insensitivity to LBIF was concomitant with the appearance of gamma + B lymphocytes. Thus, by employing LBIF as a probe, this study showed a correlation between the pathogenesis of MRL autoimmune disease and the lack of LBIF sensitivity of hyperactive B lymphocytes and suggested that the intrinsic abnormality of autoimmune MRL B lymphocytes might be confined to gamma- but not mu- or alpha-committed B cells.

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Molecular aspects of autoimmunity

Cited by 11 publications

References 25 publications

CD4⁺, CD8⁺, and CD4⁻ CD8⁻ T Cells in CSF and Blood of Patients with Multiple Sclerosis and Tension Headache

CD4⁺, CD8⁺, and CD4⁻ CD8⁻ T Cells in CSF and Blood of Patients with Multiple Sclerosis and Tension Headache

Correlations of autoimmunity with H2 and T cell receptor β chain genotypesin (NZB x NZW) F₂ mice

Abnormal behavior of γ‐committed B lymphocytes probed by a lymphocyte blastogenesis inhibitory factor in autoimmune MRL mice

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Molecular aspects of autoimmunity

Cited by 11 publications

References 25 publications

CD4+, CD8+, and CD4− CD8− T Cells in CSF and Blood of Patients with Multiple Sclerosis and Tension Headache

CD4+, CD8+, and CD4− CD8− T Cells in CSF and Blood of Patients with Multiple Sclerosis and Tension Headache

Correlations of autoimmunity with H2 and T cell receptor β chain genotypesin (NZB x NZW) F2 mice

Abnormal behavior of γ‐committed B lymphocytes probed by a lymphocyte blastogenesis inhibitory factor in autoimmune MRL mice

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CD4⁺, CD8⁺, and CD4⁻ CD8⁻ T Cells in CSF and Blood of Patients with Multiple Sclerosis and Tension Headache

CD4⁺, CD8⁺, and CD4⁻ CD8⁻ T Cells in CSF and Blood of Patients with Multiple Sclerosis and Tension Headache

Correlations of autoimmunity with H2 and T cell receptor β chain genotypesin (NZB x NZW) F₂ mice