ISSN:0891-6934    

DOI:10.3109/08916938909043608

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

We have previously reported that lymphoid cells from systemic lupus erythematosus (SLE) mice with established disease migrate aberrantly.1This study evaluates the abnormal lymphocyte migration patterns found in MRL-lpr/lpr (MRL/1) mice in relation to age, disease manifestations and the expression of lymphocyte homing receptors,51chromium-labelled lymph node cells from MRL/1 and from normal histocompatible CBA mice of different ages were injected i.v. into age and sex-matched CBA recipients. Diminished lymph node and increased hepatic uptake of MRL/1 compared to CBA cells was evident as early as 6 weeks of age. Abnormalities in lymphocyte migration antedated the appearance of elevated antihistone antibody (AHA) levels but not the development of lymphadenopathy. Using the monoclonal antibody MEL-14, no differences in the expression of lymphocyte homing receptors between MRL/1 and CBA lymph node cells were found at any age. Thus abnormalities in lymphocyte migration in MRL/1 mice appear as early as six weeks and are not related to changes in homing receptor expression.

ISSN:0891-6934    

DOI:10.3109/08916938909043609

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

We have previously described a monoclonal antibody, B16G, which has been found to be specific for T-cell derived suppressor factors (TsF). B16G has been shown to react with T-suppressor cells, TsF in the spleen of normal or tumor-bearing mice, the TsF produced by tumour-specific, or hapten-specific T-cell hybridomas, and with polyclonal whole human TsF isolated from tonsillar tissue. This pan-reactivity inherent to the B16G antibody suggests that it recognizes some common, shared epitope of the TsF molecule. In this study, we have used B16G as a probe to isolate a TsF-producing T-cell hybridoma, S-50, from CBA mice (H-2k) that is specific for the Lupus-associated antigen, RNP-Sm. The TsF bound specifically to RNP-Sm and inhibited the production of anti-RNP-Sm antibody cell cultures from MRL-lpr mice. SDS-PAGE analysis of purified S-50 TsF revealed a B16G-reactive band with a molecular weight of43kd.

ISSN:0891-6934    

DOI:10.3109/08916938909043610

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

Adult and one week old marmosets were injected intravenously within a one month period or intraperitoneally within a 6 week period respectively, with monoclonal IgM having an anti-myelin associated glycoprotein antibody activity. No clinical or electrophysiological abnormalities could be detected in experimental animals. However, indirect immunofluorescence studies showed IgM deposition in close contact to myelin sheaths. Minor but distinct alterations of nerves werre found in the adult: the enlargement of Schmidt-Lanterman incisures seen in electron microscopy could explain the decrease of the proportion of fibers of small diameter found by morphometry of semi-thin section, and the reduction of the mean internodal length in fibers of a given diameter seen in teased nerve fibers studies.

ISSN:0891-6934    

DOI:10.3109/08916938909043611

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

Cells suppressing red blood cell (RBC) autoantibody responses were found to exert their effect in Lyt-2+depleted recipients. Mice injected with monoclonal antibodies to Lyt-2 became deficient in Lyt-2+cells as judged by indirect immunofluorescence. These mice and normal recipients were given either rat RBC primed spleen cells (suppressor cells) or normal spleen cells and challenged with rat RBC. The autoantibody response of both Lyt-2+depleted and normal recipients was suppressed as compared with that of mice given normal spleen cells. It is suggested that an Lyt-1+cell may be involved in the expression of suppression.

ISSN:0891-6934    

DOI:10.3109/08916938909043612

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

Thymus-dependent (T) lymphocytes predominantly recognize antigens only when associated with products of the major histocompatibility complexes (MHC). This phenomenon is known as“genetic restriction”of the immune response. MHC Class II antigens restrict immunoregulatory T cells whereas Class I molecules determine the recognition by cytotoxic T cells or tumor cells and virus-infected cells. Genetic variations in cell-mediated and humoral responses to antigens have been related to variations in the first extracellular domain of Class II molecules.1The bulk of data relate to the mouse, but similar information relative to the human is rapidly emerging.

ISSN:0891-6934    

DOI:10.3109/08916938909043613

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

Most current theories to explain autoimmunity either implicate dysregulation within the immune system as the cause, and regard the diseased tissue as the victim,1,2or speculate on idiotype anti-idiotype cross-reactions.3,4There are objections to both views. The hypothesis presented here argues that autoimmunity is not itself an entity, but a physiological response to sustained excess antigen turnover in diseased tissues (the primary lesion) and fundamentally no different from the response to foreign antigen. Those who develop clinical disease are viewed as high responders to critical antigens. High responder status is determined by immune response (HL-linked) genotype, not immune dysregulation.

ISSN:0891-6934    

DOI:10.3109/08916938909043614

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

ISSN:0891-6934    

DOI:10.3109/08916938909043615

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

ISSN:0891-6934    

DOI:10.3109/08916938909043616

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor