CBA/N X-linked B-cell defect prevents NZB B-cell hyperactivity in F1 mice.

Taurog, Joel D.; Moutsopoulos, Haralampos Μ.; Rosenberg, Yvonne J.; Chused, Thomas M.; Steinberg, Alfred D.

doi:10.1084/jem.150.1.31

Cited by 69 publications

(24 citation statements)

References 30 publications

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“…This 4-d antibody response to rI. rC has been previously shown to be absent in CBA/N-defective mice (31,38).…”

Section: Methodsmentioning

confidence: 96%

“…Single cell suspensions of individual spleens were washed three times through fetal calf serum (FCS), then cultured in replicate 1-ml aliquots containing 107 nucleated cells in modified Mishell-Dutton medium, as previously described (38). Precuhure and 4-h culture supernatant fluids were then assayed for IgM content.…”

Section: Assay Of Igmmentioning

confidence: 99%

“…Briefly, dilutions of serum in PBS, containing 0.5% rabbit serum albumin, were incubated in microtiter wells previously coated with BGG, 10 #g/ml in PBS. After rinsing, the wells were incubated with affinity-purified 3H-rabbit anti-mouse Ig (9, 38), then rinsed and individually counted for 3H (9,38). The antibody response of tolerized and challenged mice was expressed as a percentage of the response of mice not tolerized, hut challenged.…”

Section: Assay Of Igmmentioning

confidence: 99%

“…Heparinized erythrocytes were washed and assayed for agglutination with serial dilutions of sheep antimouse Ig serum, as previously described (14,38). Known positive and negative controls were included in each assay and gave expected results.…”

Section: Assay Of Igmmentioning

confidence: 99%

“…Culture supernatant fluids and serum sample were assayed for IgM levels by solid phase radioimmunoassay, as previously described (38). Briefly, flexible roundbottom microtiter plates were coated with 10 #g/ml afflnity-purified rabbit anti-mouse Ig in phosphatebuffered saline (PBS).…”

Section: Assay Of Igmmentioning

confidence: 99%

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T cell abnormalities in NZB mice occur independently of autoantibody production.

Taurog¹,

Raveché²,

Smathers³

et al. 1981

The Journal of Experimental Medicine

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New Zealand Black (NZB) 1 mice spontaneously develop an autoimmune disease characterized by autoantihodies to erythrocytes, T lymphocytes, and nucleic acids. Death due to hemolytic anemia, lymphoid malignancy, or immune complex nephritis occurs at a mean of 15-18 mo of age (1-4). Both the B and T cell populations of NZB mice have been shown to manifest abnormal immune functions (2-18). However, NZB mice spontaneously produce IgM anti-T cell antibodies beginning early in life (19)(20)(21)(22). Moreover, such antibodies preferentially interact with, and eliminate, suppressor ceils (23-26). Thus, anti-T cell antibodies, the products of B cells, have been postulated to bring about T cell abnormalities in NZB mice (21)(22)(23)(24)(25)(26).CBA/N mice bear an X-linked gene (xid) which results in the lack of a subpopulation of B cells that normally appears late in ontogeny (27-44). We (38) and others (39) have demonstrated that the xid is completely expressed in CBA/N × NZB F1 males. However, other workers have reported autoantibody production by CBA/N X NZB males (45). Unfortunately, the contribution to the full expression of NZB autoimmune disease of the B cell subset controlled by xid cannot be explored in CBA/N × NZB F1 hybrids because these mice, as well as female CBA/N × NZB and male NZB x CBA/N mice, produce only low levels of autoantibodies, and live a normal life span of 2 yr or more (A. D. Steinberg and J. P. Reeves, unpublished observations). Therefore, to explore adequately the natural history ofxid-bearing NZB mice, we have studied congenic mice bearing the xid on an NZB background. Study of these mice has permitted us to shed further light on the pathogenesis of autoimmunity in NZB mice. Furthermore, because such mice failed to produce autoantibodies, we were able to study T cell function in the absence of autoantibody production.

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“…This 4-d antibody response to rI. rC has been previously shown to be absent in CBA/N-defective mice (31,38).…”

Section: Methodsmentioning

confidence: 96%

Section: Assay Of Igmmentioning

confidence: 99%

Section: Assay Of Igmmentioning

confidence: 99%

Section: Assay Of Igmmentioning

confidence: 99%

Section: Assay Of Igmmentioning

confidence: 99%

See 3 more Smart Citations

T cell abnormalities in NZB mice occur independently of autoantibody production.

Taurog¹,

Raveché²,

Smathers³

et al. 1981

The Journal of Experimental Medicine

Self Cite

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Approach to the study of the role of sex hormones in autoimmunity

Steinberg

Melez

Raveché

et al. 1979

Arthritis & Rheumatism

180

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Investigators from this laboratory have been studying sex hormones in normal and autoimmune mice for the past 10 years. We have found that immune responses to DNa are influenced by sex hormones. Androgens reduce and estrogens increase both spontaneous and immunization-induced antibodies to single-stranded DNA in NZB X NZW, NZB X C3H, NZB X CBA, NZB X DBA mice. Treatment of female NZB/W mice with testosterone or 5 alpha dihydrotestosterone retards the progress of autoimmunity. Castration is not necessary for this effect. In contrast, danazol has no favorable effect on the disease process. Estrogens cause a marked acceleration of autoimmunity and a reduction in thymus weight. During the course of these studies, we found that a number of problems or variables arise in studying sex hormone effects, including: 1) X-linked genes, 2) metabolism of testosterone to estrogens, 3) dose of hormone, 4) age at which administration is initiated, 5) differential effects of sex hormones on different autoantibodies and various immune responses.

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Studies of immune functions of patients with systemic lupus erythematosus

Sakane

Green

1980

Arthritis & Rheumatism

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Genetic, environmental, and immune factors have been implicated in the pathogenesis of active systemic lupus erythematosus (SLE). To investigate the basis for abnormalities in immune regulation, we studies lymphocytes from patients with SLE during the active and inactive phases of their disease to examine their ability to develop Con A induced suppressor function (5 patients) and to develop a normal autologous mixed lymphocyte reaction (MLR) (7 patients). In each case results of these in vitro tests using whole T cells were abnormal during the active phase of the disease and returned to normal when the disease activity decreased. The results of this study suggest that the abnormalities of suppressor cell generation and the autologous MLR observed in whole T cell populations from patients with active SLE are not solely due to intrinsic and invariant lymphocyte defects. They further suggest that loss of immune regulatory function is not a simple genetically determined trait since the regulatory function returned to normal when the disease became inactive. However, these results do not exclude an underlying genetic effect on the immune system which requires a second factor (such as an environmental trigger) for expression. Evidence in support of this latter possibility derives from studies of Tγ cells. Fractionation of the functionally normal whole T cells from some patients who were clinically inactive revealed impaired function of Tγ cells. This subset of T cells may be easily perturbed by stimuli not sufficient to cause clinically apparent disease.

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CBA/N X-linked B-cell defect prevents NZB B-cell hyperactivity in F1 mice.

Cited by 69 publications

References 30 publications

T cell abnormalities in NZB mice occur independently of autoantibody production.

T cell abnormalities in NZB mice occur independently of autoantibody production.

Approach to the study of the role of sex hormones in autoimmunity

Studies of immune functions of patients with systemic lupus erythematosus

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