Rosette formation between murine lymphocytes and erythrocytes. A new locus in the H-2 region.

Primi, Daniélé; Lewis, G K; Triglia, Richard P.; Goodman, Joel W.

doi:10.1084/jem.149.6.1349

Cited by 32 publications

(8 citation statements)

References 22 publications

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“…Our results confirm three previous reports (Charreire et al, 1980;Sia and Parish, 1980a;Primi et al, 1979) that lymphocyte-erythrocyte rosetting shows self-MHC preference. However, our results differ from all these reports in that we found that complete identity at class I MHC was required for maximum rosette frequency, whereas they found that partial identity was sufficient.…”

Section: Discussionsupporting

confidence: 96%

“…Probably not. Primi et al (1979) observed it for cultured splenocytes. Sia and Parish (1980b) observed it for splenocytes (primarily B cells), lymph node cells, and bone marrow cells as well as for thymocytes.…”

Section: Discussionmentioning

confidence: 95%

“…Antibody against CD3 did not inhibit rosette formation (Table 4). In addition, B cells can form MHC-specific rosettes in a process not involving surface immunoglobulin (Sia and Parish 1980a,b;Primi et al, 1979). Some as yet uncharacterized set of adhesion molecules would appear to be primarily involved.…”

Section: Discussionmentioning

confidence: 99%

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Dependence of mouse thymocyte‐erythrocyte rosette formation on complete identity at class‐l‐MHC

Sem

Sambhara

Chadwick

et al. 1991

Journal Cellular Physiology

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Mouse thymocytes and erythrocytes form rosettes when incubated together at 4 degrees C. The frequency is much higher when the thymocytes and erythrocytes are MHC-identical. If the indolizidine alkaloid swainsonine (SW) is present during rosette formation at concentrations of 1 microgram/ml (5.7 microM) or greater, rosette formation between MHC-identical pairs is inhibited to levels comparable to those observed for MHC-different pairs; rosette formation by MHC-different pairs is not affected. This was confirmed by examining 17 different MHC-identical combinations (9 completely syngeneic and 8 differing in non-MHC genes) and 13 MHC-different combinations (3 of these identical everywhere except at MHC). A SW-inhibitable component of rosette formation was observed only when thymocyte and erythrocyte were completely identical at MHC. Thus F1-parent pairs behaved as if allogeneic, although both F1-F1 and parent-parent had a SW-inhibitable rosetting component. Similarly, inbred strains only partially MHC-identical (B10.BR-B10.A, B10.D2-B10.A) behaved as if allogeneic. The SW-inhibitable component of rosetting could be partially but significantly blocked by including monoclonal antibodies against Thy-1, and anti-CD4 plus anti-CD8 (together but not separately); anti-class-I-MHC produced some inhibition of marginal significance. Monoclonal antibodies against class-I-MHC, LFA-1, and CD3 did not block. Pretreatment of erythrocytes with neuraminidase, greatly reduced the SW-inhibitable component of rosetting. The SW effect would appear to be due to a direct interaction of SW with a cell surface structure involved in syngeneic rosette formation rather than the known ability of SW to block the processing of N-linked sugar structures. The results are consistent with cell surface lectins and cell surface sugars playing a role in rosette formation.

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Section: Discussionsupporting

confidence: 96%

Section: Discussionmentioning

confidence: 95%

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Dependence of mouse thymocyte‐erythrocyte rosette formation on complete identity at class‐l‐MHC

Sem

Sambhara

Chadwick

et al. 1991

Journal Cellular Physiology

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“…In this species, however, the ability to form rosettes requires histocompatibility in the L region between the T lymphocyte and the mouse erythrocytes (28)(29)(30). No functional studies of the ARFT-forming T cell subset in the mouse have yet been reported.…”

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confidence: 99%

Autologous rosette-forming T cells regulate responses of T cells. Phenotypic and functional analysis of suppressor cells generated from autologous rosette-forming T cells after autologous mixed lymphocyte reactions.

Kumagai¹,

Scher²,

Green³

1981

J. Clin. Invest.

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A B S T R A C T An average of 5-9% of human peripheral blood of T lymphocytes form rosettes with autologous erythrocytes (ARFT). This population responded only slightly against autologous and allogeneic non-T cells. In contrast, T cells that did not form rosettes with autologous erythrocytes (NRFT) proliferated to a greater degree in auto-and allogeneic mixed lymphocyte reactions (MLR) and also in reactions to trinitrophenyl (TNP) modified autologous non-T cells (TNP-auto-MLR) as compared with ARFT or unfractionated T cells. The ARFT populations could suppress the increased allogeneic (allo)MLR and TNPauto-MLR of NRFT when the ARFT were added to the NRFT at the beginning of the cultures.Fluorescence-activated cell-sorter (FACS) analysis of these freshly obtained T cell fractions using monoclonal antibodies to subpopulations of T cells did not demonstrate any selective gain or loss of T cell subsets in the ARFT and NRFT as compared with unfractionated T cells. But when each T cell fraction was cultured separately for a week in the presence of autologous non-T cells (auto-MLR) and the cells were again analyzed' by fluorescence-activated cell sorter, there was an increase in OKT8-positive cells (suppressor/cytotoxic subset) only in the ARFT fraction. The above findings strongly suggest that suppressor T cells are generated from the ARFT fraction during an auto-MLR, these may then regulate the responses of NRFT.

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“…T,, cells are also the precursors of natural killer cells in autologous mixed lymphocyte reaction (20) and behave as responding cells in this autologous reaction (2 1). In the mouse, autologous erythrocyte rosettes are formed by both B and T cells (22). This does not seem to be the case in humans where anti-T, but not anti-B serum, blocks autologous rosette formation (18).…”

Section: Discussionmentioning

confidence: 99%

Human Postthymic Precursor Cells in Health And Disease

Alarcón‐Segovia¹,

Palacios²

1981

Arthritis & Rheumatism

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Human T cells are capable of forming rosettes with autologous erythrocytes (Tur cells) and behave as postthymic precursors. Thus, they generate T, and T, cells as well as suppression and spontaneous cytotoxicity and participate in a pokeweed mitogen-driven system akin to that of feedback inhibition in which murine postthymic precursors participate. T,,, cells were increased in 7 patients with mixed connective tissue disease (MCTD) compared to normal agelsex-matched controls. Despite this increase of precursor cells, decreased T, cells and abrogation in the generation of suppression and of feedback inhibition were noted. These functional defects were not correctable with serum thymic factor but could be corrected by the addition of either allogenic T, or mononuclear cells depleted of T,, cells. Our findings suggest that the immunoregulatory T cell circuits in MCTD may be adequate both in postthymic precursor cells and in the thymic factor prompting. They are probably abnormal either at the site of T, signaling to T,, cells in feedback inhibition or in the T, reception of suppressor signals from T, cells. The decrease of T, cells in MCTD could be due to the decreased stimulus from feedback inhibition andor to the penetration of anti-ribonucleoprotein antibody. Abnormalities of immunoregulatory T cell circuits in MCTD are quite different from those found previously in systemic lupus erythematosus, scleroderma, and rheumatoid arthritis. These differences support the notion that MCTD is a distinct entity. Controversy exists about whether mixed connective tissue disease (MCTD) is a distinct entity or a subset of systemic lupus erythematosus (SLE) (1-3).In both diseases, patients have decreased circulating T, cells (1,4) and loss of suppressor cell function (1,5,6). Patients with SLE, however, may show a heterogeneity between the results of spontaneously expanded and concanavalin A (Con A) induced suppressor cell functions (7), whereas both of these functions are decreased homogeneously in MCTD (1).Spontaneously expanded and Con A-induced suppressor functions are generated by postthymic precursor cells which are distinguishable as well as separable in humans by their property of forming rosettes with autologous erythrocytes (8). Circulating mononuclear cells (MNC) from patients with SLE have decreased proportions of autologous rosetteforming T cells (Tu, cells) and T,, cells from SLE patients have a decreased capacity of generating suppression (9). Cells from SLE patients also function poorly in a pokeweed mitogen (PWM) driven system where T,, cells provide suppression under the influence of T, cells and help under the influence of T, cells. This functional property resembles murine feedback inhibition which can be defined as the induction of T suppression on B cells by helper T cells signaling unprimed postthymic precursor T cells (9); thus we have designated this phenomenon human feedback inhibition. These abnormalities of the T,, cells from the peripheral blood of SLE patients are partially correctable with serum th...

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Rosette formation between murine lymphocytes and erythrocytes. A new locus in the H-2 region.

Cited by 32 publications

References 22 publications

Dependence of mouse thymocyte‐erythrocyte rosette formation on complete identity at class‐l‐MHC

Dependence of mouse thymocyte‐erythrocyte rosette formation on complete identity at class‐l‐MHC

Autologous rosette-forming T cells regulate responses of T cells. Phenotypic and functional analysis of suppressor cells generated from autologous rosette-forming T cells after autologous mixed lymphocyte reactions.

Human Postthymic Precursor Cells in Health And Disease

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