B Cell Differentiation Antigens as Probes for Functional B Cell Subsets

Huber, Brigitte

doi:10.1111/j.1600-065x.1982.tb00418.x

Cited by 31 publications

(7 citation statements)

References 60 publications

(37 reference statements)

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“…W39). It is not clear why such cells were apparently not stimulated to a significant extent when (CBA/N x C57BL/6)Fl hybrids (male or female) were primed with PI or BI as reported by Rosenwasser and Huber [7,81. This discrepancy could be due to the immunization procedure or technical differences in the assay system.…”

Section: Discussionmentioning

confidence: 77%

“…W39-carrying I-Ah molecules are not required as components of the F1-unique restriction element recognized by the ST2 T cells in conjunction with PI, BI, SI, or HI. Due to a mutation on the X chromosome of CBA/N mice cells of male (CBA/N x C57BL/6)F1 hybrids do not express Ia.W39, aprivate specificity of I-Ah, on their membrane [7]. Ia molecules carrying this specificity have been reported to be essential for the recognition of BI by T cells of (CBA/N x C57BL/6)F1 hybrids or of the C57BL/6 parental strain [7, 81. For instance, male (CBA/N x C57BL16)F1 hybrids not expressing Ia.W39 were found to be nonresponsive to BI, as measured by T cell proliferation and accessory cells of these male F1 hybrids, in contrast to those of females, could not present BI to primed T cells of the female hybrids.…”

Section: Biobr)f1 T Cell Line St2 Restimulation Of T Cells Was Foundmentioning

confidence: 99%

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Epitope specificity and Ia restriction of T cell responses to insulin in a system of complementing Ir genes: analysis with primed lymph node T cells and a long‐term cultured T cell line

Spaeth

Rüde

1983

Eur J Immunol

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The antibody response of (H-2b X H-2k)F1 mice to pig insulin (PI) has previously been shown to be under the control of H-2-linked, complementing Ir genes. In addition, this response was reported to depend on the genetic background of the parental strains (Keck, K., Eur. J. Immunol. 1977. 7: 811). Here it is demonstrated that the secondary in vitro response of proliferating T cells shows the same dependence on H-2-linked Ir genes yet an influence of the background genes could not be detected. The complementing genes were mapped to the Kb, I-Ab and Kk, I-Ak regions. For restimulation of F1 T cells by PI, the Ir genes of both parental chromosomes have to be expressed in the same antigen-presenting cell, suggesting complementation at the molecular rather than at a cell interaction level. With a long-term cultured, PI-specific T cell line (ST2) of (B10 X B10.BR)F1 origin the complementation data could be confirmed by mapping the Ia restriction elements to Kb, I-Ab and I-Ak. The reactivity pattern of this line towards species variants of insulin and the isolated A and B polypeptide chains in the presence of syngeneic accessory cells suggests that the glutamic acid residue in position 4 of the A polypeptide chain (Asp in mouse insulin) is essential for recognition in conjunction with an (I-Ab X I-Ak)F1 hybrid Ia complex. I-Ab-encoded molecules carrying specificity Ia. W39 which, according to Rosenwasser, L. J. and Huber, B. T. are essential for the presentation of BI to (CBA/N X C57BL/6)F1 T cells, are not required as components of the F1-unique restriction element recognized by the F1 T cells of the ST2 line in conjunction with PI. This is indicated by the fact that accessory cells of (CBA/N X B10)F1 hybrids, regardless of their sex, could present PI as well as beef, sheep and horse insulin to the F1-restricted ST2 cells.

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Section: Discussionmentioning

confidence: 77%

Section: Biobr)f1 T Cell Line St2 Restimulation Of T Cells Was Foundmentioning

confidence: 99%

Epitope specificity and Ia restriction of T cell responses to insulin in a system of complementing Ir genes: analysis with primed lymph node T cells and a long‐term cultured T cell line

Spaeth

Rüde

1983

Eur J Immunol

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“…The xid gene determines a well known B lymphocyte immunodeficiency: B cells of CBA/N mice show many features of immature B lymphocytes, i.e. the absence of Lyb-3, Lyb-5, Lyb-7 markers, high density of membrane IgM molecules, inability to respond to Mls-superantigen in MLC reaction [34][35][36][37]. In addition, xid-bearing mice possess a decreased quantity of antibody-forming cells of several classes (IgM, IgG1, IgG2a, IgG2b), and express a decreased proliferative response to peptidoglycan, lipopolysaccharide (LPS), protein A and PWM [38].…”

Section: Discussionmentioning

confidence: 99%

Influence of the mouse Bcg Tbc-1 and xid genes on resistance and immune responses to tuberculosis infection and efficacy of bacille Calmette–Guérin (BCG) vaccination

Никоненко

Apt

Mezhlumova

et al. 1996

Clinical and Experimental Immunology

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SUMMARYWe have studied the role of three mouse distinct non-H-2 genes (Bcg, Tbc-1, xid ) in several phenomena of antituberculosis immunity and resistance. On the basis of median survival time (MST) of mice following infection with virulent Mycobacterium tuberculosis H37Rv, Bcg gene did not control resistance to the lethal dose of H37Rv infection in non-vaccinated and Myco. bovis (BCG)-vaccinated mice. However, Bcg r allele, in comparison with Bcg s allele, determined more effective suppression of an early multiplication in spleens of H37Rv mycobacteria after a low dose (5 2 10 4 colony-forming units (CFU)) injection. CBA/N mice, which are not protected efficiently against tuberculous challenge by BCG vaccination, were characterized by a decreased in vitro proliferation of immune lymph node cells, both spontaneous and stimulated with mycobacterial antigens. The decreased proliferation was due to immunosuppression caused by interactions between responding T cells and CBA/N antigen-presenting cells (APC). We have confirmed that the defective response to BCG-vaccination in CBA/N mice is linked with the X-chromosome and thus is presumably determined by the xid gene itself. I/St mice (Tbc-1 s ), supersusceptible to H37Rv infection, were not able to restrict the growth of H37Rv mycobacteria in spleens, even following infection with a low dose (5 2 10 4 ), but restricted the growth of Myco. bovis BCG more effectively than Bcg s mice.

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“…Thus, it is possible that in an analogous fashion there is a variant of sIgM that accounts for the H-40 epitope. In a different system, Huber (31) has defined an epitope, Iaw.39, which is expressed on the I-A b molecule. This epitope is not found in (CBA/N ~ x C57BL/6 ~)Fl animals, even though they possess a normal LA b gene.…”

Section: Discussionmentioning

confidence: 99%

H-40, an antigen controlled by an Igh linked gene and recognized by cytotoxic T lymphocytes. I. Genetic analysis of H-40 and distribution of its product on B cell tumors.

Forman¹,

Riblet

Brooks

et al. 1984

The Journal of Experimental Medicine

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The lgh complex is on the murine 12th chromosome and contains the genes (Igh-C) that encode the constant (C) portion of/~, 6, 3', a, and e immunoglobulin (Ig) heavy chains together with J, D, and V region genes that encode their corresponding variable (V) regions (1-3). In addition to these Igh genes, there are several other linked genes, some of which may play a role in immune reactivity. For example, a series of antigens have been described: Tsu, Tind, Tthy, and Tpre, which are controlled by genes that map telomeric to the lgh locus (reference 4, and R. Riblet, E. Eicher, and B. Taylor, unpublished data). These antigens are limited in their tissue expression to T cell subsets and have been detected on T cell factors that have immunoregulatory activity (5-7). Lyb-7 is an antigenic determinant controlled by a gene linked to the lgh-V side of the complex and is selectively expressed on a B lymphocyte subset (8). In contrast, the lgh-linked minor histocompatibility H(Igh) (9) and prealbumin (Pre-1) genes (10) presumably encode molecules that are unrelated to the immune system.

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B Cell Differentiation Antigens as Probes for Functional B Cell Subsets

Cited by 31 publications

References 60 publications

Epitope specificity and Ia restriction of T cell responses to insulin in a system of complementing Ir genes: analysis with primed lymph node T cells and a long‐term cultured T cell line

Epitope specificity and Ia restriction of T cell responses to insulin in a system of complementing Ir genes: analysis with primed lymph node T cells and a long‐term cultured T cell line

Influence of the mouse Bcg Tbc-1 and xid genes on resistance and immune responses to tuberculosis infection and efficacy of bacille Calmette–Guérin (BCG) vaccination

H-40, an antigen controlled by an Igh linked gene and recognized by cytotoxic T lymphocytes. I. Genetic analysis of H-40 and distribution of its product on B cell tumors.

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