Decreased autologous mixed lymphocyte reaction in Sjögren's syndrome.

Miyasaka, Nobuyuki; Sauvezie, B; Pierce, Donald A.; Daniels, T.; Talal, Norman

doi:10.1172/jci109960

Cited by 138 publications

(50 citation statements)

References 25 publications

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“…Analogous results have been reported in patients with SLE (Sakane et al 1978) and Sjogren's syndrome (Miyasaka et al 1980) and in the SLE model in NZB mice (Smith and Pasternak 1978). Although the exact biologic role of the AMLR has not been fully established, it is assumed to reflect an important immunoregulatory function (Opelz et al 1975;Kuntz et al 1976;Sakane et al 1978).…”

Section: Autologous Mixed Lymphocyte Reaction (Amlr)supporting

confidence: 82%

“…Recently, autologous mixed lymphocyte reaction (AMLR), in which human T cells respond with increased DNA synthesis to mitomycin-C treated or x-irradiated non-T cells, is employed to investigate the immunoregulatory function of T cells (Kuntz et al 1976;Sakane et al 1978). AMLR was found to be decreased in SLE (Sakane et al 1978) and in Sjogren's syndrome (Miyasaka et al 1980). The purpose of the present investigation is to obtain more precise knowledge of immunoregulatory function in patients with CAR.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Studies of immune functions of patients with chronic hepatitis.

Nonomura

Tanino

Kuroda

et al. 1982

Tohoku J. Exp. Med.

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Section: Autologous Mixed Lymphocyte Reaction (Amlr)supporting

confidence: 82%

mentioning

confidence: 99%

Studies of immune functions of patients with chronic hepatitis.

Nonomura

Tanino

Kuroda

et al. 1982

Tohoku J. Exp. Med.

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“…However, that study used fetal calf serum, which has been shown to augment proliferation without affecting IL-2 production in the syngeneic mixed lymphocyte response (5). A suppressed AMLR has been observed in 3 other studies (33)(34)(35)(36)(37)(38)(39), and 1 of these showed an association with disease activity. In our study, those patients with the most active, severe disease had the most consistent and severe defects.…”

Section: Discussionmentioning

confidence: 69%

“…Separation of mononuclear cells. Sixty milliliters of peripheral venous blood was collected in heparin (25 units/ ml; Gibco, Grand Island, NY) (39). Blood was diluted with an equal volume of RPMI 1640 (Gibco) containing 2 mM glutamine, 10 mM HEPES, 100 unitdm1 penicillin, 100 CLglml streptomycin, 25 kg/ml fungizone, and 50 mg/ml gentamicin (termed semicomplete media).…”

Section: Methodsmentioning

confidence: 99%

Characterization of the defective autologous mixed lymphocyte response in rheumatoid arthritis

Pope

Mcchesney

Talal

et al. 1984

Arthritis & Rheumatism

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In order to characterize the autologous mixed lymphocyte response (AMLR) in patients with rheumatoid arthritis (RA) and to define the relationship with disease activity, peripheral blood T lymphocytes were stimulated with either a B lymphocyte-enriched (B cells) or a macrophage-enriched (macrophages) population. A significant reduction (P < 0.01 to P < 0.001) of T cell proliferation stimulated both by B cells and macrophages was observed in patients with active disease. The B lymphocytes were significantly less stimulatory (P < 0.02 to P < 0.001) than macrophages in the patients compared with the controls. In the normal controls, macrophages in higher concentrations were capable of suppressing the B lymphocyte-stimulated AMLR, but macrophages from patients with RA were not excessively suppressive. A significant association (P < 0.02) was observed between disease activity and the AMLR. Using the B-enriched population, the AMLR proliferative response was significantly associated (P < 0.001) with the production of interleukin-2. Defects in proliferation could only be partially restored by the addition of interleukin-2. These data indicate that the defective AMLR observed in patients with RA is related to disease activity and is associated with altered cellular interac- The autologous mixed lymphocyte response (AMLR) is a proliferative response of T lymphocytes to autologous non-T cells (1,2). This response is dependent upon the recognition of class I1 histocompatibility antigens on the surface of the accessory cells (3-6). Macrophages, B lymphocytes, dendritic cells, and null cells are capable of stimulating the AMLR (1,3,(7)(8)(9)(10). Recently, even a subset of la-positive T lymphocytes has been shown to be capable of stimulating an AMLR (11). The AMLR is specific and has been shown to possess memory (12). It is capable of generating both T lymphocyte help and suppression and of augmenting cytotoxicity and natural killer activity (12- 21).The AMLR may represent an in vitro model of in vivo cellular communication capable of generating interleukin-2 (IL-2) in an antigen-independent fashion (5). As such, it may serve as an important model for examining the defective cellular interactions responsible for a number of autoimmune disorders. Although claims have been made that the AMLR is primarily due to xenogenic antigens employed in isolation techniques (22,23), the work of numerous investigators (5,(24)(25)(26), as well as our own unpublished observations, have demonstrated that the AMLR is not due solely to foreign antigens, although such antigens are capable of augmenting the response.A defective AMLR has been described in a Submitted for publication December 12, 1983; accepted in number of autoimmune, immune deficiency, and neoplastic disorders (27-31, reviewed in 32). The data concerning the AMLR in patients with rheumatoid arthritis (RA) are conflicting regarding both the pres-

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“…Recently, autologous mixed lymphocyte reaction (AMLR), in which human T cells respond to mitomycin-C treated or X-irradiated autologous non-T cells, is employed to investigate immunoregulatory functoins (Sakane and Steinberg 1978). AMLR was found to be decreased in patients with systemic lupus erythematosus (Sakane and Steinberg 1978), Sjogren's syndrome (Miyasaka et al 1980) and chronic activie hepatitis (Nonomura et al 1982 …”

mentioning

confidence: 99%