scholarly journals Adoptive transfer of neonatal T lymphocytes rescues immunoglobulin production in mice with severe combined immune deficiency.

1991 ◽  
Vol 173 (1) ◽  
pp. 265-268 ◽  
Author(s):  
J E Riggs ◽  
R S Stowers ◽  
D E Mosier
Keyword(s):  
Immune Deficiency ◽  
T Cells ◽  
T Cell ◽  
B Cells ◽  
Autosomal Recessive ◽  
Low Frequency ◽  
Cell Receptor ◽  
Scid Mice ◽  
Severe Combined Immune Deficiency ◽  
Combined Immune Deficiency

Mice with the autosomal recessive severe combined immune deficiency (scid) mutation lack mature lymphocytes because of defective joining of T cell receptor and immunoglobulin (Ig) gene segments. Penetrance of this mutation is incomplete since 10-25% of SCID mice produce some T or B lymphocytes. This "leaky" phenotype could be due to a reversion of the mutation in some mice or to a constant, low frequency of functional lymphocytes generated in all SCID mice with variable survival of such cells. We report here that all SCID mice can be stimulated to produce functional B cells by the transfer of normal neonatal, but not adult, T cells. T cell-induced rescue of C.B-17scid B cells results in high levels of Ig expressing the Ighb allotype of the SCID recipient. These results show that all SCID mice generate some functional B cells, the majority of which do not survive in the absence of a subset of T cells present in high frequency in the neonate.

scholarly journals T cell-independent antibody-mediated clearance of polyoma virus in T cell-deficient mice.

1996 ◽  
Vol 183 (2) ◽  
pp. 403-411 ◽  
Author(s):  
E Szomolanyi-Tsuda ◽  
R M Welsh
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cells ◽  
Nude Mice ◽  
Knockout Mice ◽  
Cell Receptor ◽  
Genetically Engineered ◽  
Scid Mice ◽  
Myeloproliferative Disease ◽  
Alpha Beta

Polyomavirus (PyV) infection of SCID mice, which lack functional T and B cells, leads to a lethal acute myeloproliferative disease (AMD) and to high levels of virus replication in several organs by two wk after infection. This is in contrast to infection of T cell-deficient athymic nude mice, which are resistant to acute PyV-induced disease and poorly replicate the virus in their organs. This major difference in the virus load and in the outcome of PyV infection between SCID and nude mice suggested that an efficient, T cell-independent antiviral mechanism operates in T cell-deficient, PyV infected mice. To investigate this possibility, mice with different genetically engineered T and/or B cell deficiencies and SCID mice adoptively reconstituted with B and/or T cells were infected with PyV. The results indicated that the presence of B cells in the absence of T cells protected mice from the AMD, and this was accompanied by a major reduction of PyV in all organs tested. Sera from PyV-infected T cell receptor (TCR) alpha beta knockout or TCR alpha beta gamma delta knockout mice contained IgG2a antibodies to PyV. Sera or purified immunoglobulin fractions from PyV-infected TCR alpha beta knockout mice protected SCID mice from the PyV-induced AMD. To our knowledge, this is the first report of an effective T cell-independent antibody response clearing a virus and changing the outcome of infection from 100% mortality to 100% survival.

XX T cells and XY B cells in two patients with severe combined immune deficiency

1984 ◽  
Vol 31 (1) ◽  
pp. 87-95 ◽  
Author(s):  
Mary Ellen Conley ◽  
Peter C. Nowell ◽  
Gertrude Henle ◽  
Steven D. Douglas
Keyword(s):  
Immune Deficiency ◽  
T Cells ◽  
B Cells ◽  
Severe Combined Immune Deficiency ◽  
Combined Immune Deficiency

scholarly journals Evidence of functional lymphocytes in some (leaky) scid mice.

1988 ◽  
Vol 167 (3) ◽  
pp. 1016-1033 ◽  
Author(s):  
G C Bosma ◽  
M Fried ◽  
R P Custer ◽  
A Carroll ◽  
D M Gibson ◽  
...  
Keyword(s):  
Immune Deficiency ◽  
T Cells ◽  
General Pattern ◽  
Scid Mice ◽  
Lymphoid Tissues ◽  
Severe Combined Immune Deficiency ◽  
Splenic Cells ◽  
Combined Immune Deficiency ◽  
Lymphocyte Antigens ◽  
High Concentrations

Although the majority of severe combined immune deficiency (scid) mice lack functional lymphocytes, some (2-23%) appear to develop a limited number of B and T cells between 3 and 9 mo old. Most of these leaky scid mice were shown to contain very few clones (less than or equal to 3) of Ig-producing plasmacytes. Clonal progeny were distributed unevenly in the lymphatic tissues and appeared as discrete plasmacytic foci. In many cases, individual clones persisted for several months and produced abnormally high concentrations of Ig that included multiple isotypes. Functional T cells were inferred from the ability of leaky mice to reject allogeneic skin grafts, a T cell-dependent reaction. Interestingly, approximately 40% of leaky mice developed thymic lymphomas. In other respects, leaky mice resembled regular scid mice; e.g., their splenic cells failed to express common lymphocyte antigens (Ly-5[B220], Ly-1) and to proliferate in response to lymphocyte mitogens. Histologically, their lymphoid tissues retained the same general pattern of severe lymphocytic deficiency as scid mice.

An obligate role for T-cell receptor αβ+ T cells but not T-cell receptor γδ+ T cells, B cells, or CD40/CD40L interactions in a mouse model of atopic dermatitis

2001 ◽  
Vol 107 (2) ◽  
pp. 359-366 ◽  
Author(s):  
Amy L. Woodward ◽  
Jonathan M. Spergel ◽  
Harri Alenius ◽  
Emiko Mizoguchi ◽  
Atul K. Bhan ◽  
...  
Keyword(s):  
T Cells ◽  
Atopic Dermatitis ◽  
T Cell ◽  
B Cells ◽  
Mouse Model ◽  
T Cell Receptor ◽  
Γδ T Cells ◽  
Cell Receptor ◽  
Αβ T Cells

scholarly journals B2 but Not B1 Cells Can Contribute to CD4+ T-Cell-Mediated Clearance of Rotavirus in SCID Mice

2001 ◽  
Vol 75 (12) ◽  
pp. 5482-5490 ◽  
Author(s):  
Natasha Kushnir ◽  
Nicolaas A. Bos ◽  
Adrian W. Zuercher ◽  
Susan E. Coffin ◽  
Charlotte A. Moser ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Secondary Infection ◽  
Immunoglobulin A ◽  
Cell Receptor ◽  
Scid Mice ◽  
Peritoneal Exudate ◽  
Peritoneal Exudate Cells ◽  
B1 Cells ◽  
Intestinal Iga

ABSTRACT Studies utilizing various immunodeficient mouse models of rotavirus (RV) infection demonstrated significant roles of RV-specific secretory immunoglobulin A (IgA), CD4+ T cells, and CD8+T cells in the clearance of RV and protection from secondary infection. Secretion of small but detectable amounts of IgA in RV-infected αβ T-cell receptor knockout mice (11) and distinctive anatomical localization and physiology of B1 cells suggested that B1 cells might be capable of producing RV-specific intestinal IgA in a T-cell-independent fashion and, therefore, be responsible for ablation of RV shedding. We investigated the role of B1 cells in the resolution of primary RV infection using a SCID mouse model. We found that the adoptive transfer of unseparated peritoneal exudate cells ablates RV shedding and leads to the production of high levels of RV-specific intestinal IgA. In contrast, purified B1 cells do not ablate RV shedding and do not induce a T-cell-independent or T-cell-dependent, RV-specific IgA response but do secrete large amounts of polyclonal (total) intestinal IgA. Cotransfer of mixtures of purified B1 cells and B1-cell-depleted peritoneal exudate cells differing in IgA allotypic markers also demonstrated that B2 cells (B1-cell-depleted peritoneal exudate cells) and not B1 cells produced RV-specific IgA. To our knowledge, this is the first observation that B1 cells are unable to cooperate with CD4+ T cells and produce virus-specific intestinal IgA antibody. We also observed that transferred CD4+ T cells alone are capable of resolving RV shedding, although no IgA is secreted. These data suggest that RV-specific IgA may not be obligatory for RV clearance but may protect from reinfection and that effector CD4+ T cells alone can mediate the resolution of primary RV infection. Reconstitution of RV-infected SCID mice with B1 cells results in the outgrowth of contaminating, donor CD4+ T cells that are unable to clear RV, possibly because their oligoclonal specificities may be ineffective against RV antigens.

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