CBA/N Immune Defective Mice; Evidence for the Failure of a B Cell Subpopulation to be Expressed

Sche, Irwin

doi:10.1111/j.1600-065x.1982.tb00421.x

Cited by 113 publications

(42 citation statements)

References 73 publications

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“…These cells show little or no response to the (DL)BCGF preparations or other preparations that stimulated the B cells from normal (DBA/2 × CBA/N)F1 female littermates. This observation is compatible with the findings of a number of other investigators (32,33).…”

Section: Lack Of Reactivity Of B Cells From the Spleens Of X-linked Dsupporting

confidence: 82%

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Production of a B cell growth-promoting activity, (DL)BCGF, from a cloned T cell line and its assay on the BCL1 B cell tumor.

Swain¹,

Dutton²

1982

The Journal of Experimental Medicine

131

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It has long been clear that there are two components of the B cell response to antigen. There is an early phase of proliferation in which the responding B cell population is expanded many times, and a later phase of differentiation in which the already proliferating B cell moves on to the immunoglobulin-secretion stage. It has been suggested that separate signals are involved in each phase (1); it has also been realized that there must be an initial lag phase (2) before the onset of proliferation; more recent studies (3) have defined this activation step as a separate event.It has been many years since the need for a helper T cell in the B cell response to antigen was defined (4, 5) and since the demonstration that the T cell could be replaced by a helper factor (6).It is now known that a number of T cell-and macrophage-derived nonantigenspecific factors make up the activity previously defined as "helper factor." Current studies are underway to characterize each factor and to determine at which stage it acts and what is its exact role. Parker (7) has shown that B cell proliferation can be seen in cultures of positively selected B cells stimulated with anti-#. He showed that anti-# alone was not sufficient, but that interleukin 2-(IL-2) 1 containing supernatants were also required. Immunoglobulin secretion required an additional factor (or factors) not provided in IL-2, but which were present in the supernatant of concanavalin A-(Con A) stimulated T cells. Howard et al. (8; and M. Howard, personal communication) also showed that a number of factors were required for B cell proliferation. In her analysis, the extent of proliferation to anti-Ig was proportional to the third power of the B cell concentration. The slope of this curve was reduced to two by the addition of an IL-2-containing supernatant from EL4 and to nearly one by the further addition of an 18-mol wt cut from the supernatant of P388D1 (presumably, interleukin 1 [IL-1]). The B cell growth factor (BCGF) activity present in the EL4 supernatants could be separated from the IL2 activity by phenyl Sepharose

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Section: Lack Of Reactivity Of B Cells From the Spleens Of X-linked Dsupporting

confidence: 82%

“…PFC to SRBC were determined on day 4. The background PFC in cultures without TRF were 28 (24)(25)(26)(27)(28)(29)(30)(31)(32). The geometric means (±SE) of triplicate cultures is shown.…”

Section: B Cell Growth-promoting Activity and Its Assay The Results mentioning

confidence: 99%

Production of a B cell growth-promoting activity, (DL)BCGF, from a cloned T cell line and its assay on the BCL1 B cell tumor.

Swain¹,

Dutton²

1982

The Journal of Experimental Medicine

131

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“…Btk is essential at two distinct steps in B cell development in the mouse 1) at the developmental progression of CD43 ϩ CD2 Ϫ large cycling into CD43 Ϫ CD2 ϩ small resting pre-B cells and 2) at the checkpoint for selection of immature IgM high T2 cells into the pool of long-lived IgM low mature B cells (5,19,28,30,31,35,36). In this report, we show that in Btk-deficient mice premature expression of the 3-83␦ BCR amplifies the cellular maturation defects in immature B cells in the BM and results in an arrest of peripheral B cell development at the transition of T1 into T2 cells in the spleen.…”

Section: Discussionmentioning

confidence: 99%

Cellular Maturation Defects in Bruton’s Tyrosine Kinase-Deficient Immature B Cells Are Amplified by Premature B Cell Receptor Expression and Reduced by Receptor Editing

Middendorp

Hendriks

2004

The Journal of Immunology

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In the mouse, Bruton’s tyrosine kinase (Btk) is essential for efficient developmental progression of CD43+CD2− large cycling into CD43−CD2+ small resting pre-B cells in the bone marrow and of IgMhigh transitional type 2 B cells into IgMlow mature B cells in the spleen. In this study, we show that the impaired induction of cell surface changes in Btk-deficient pre-B cells was still noticeable in κ+ immature B cells, but was largely corrected in λ+ immature B cells. As λ gene rearrangements are programmed to follow κ rearrangements and λ expression is associated with receptor editing, we hypothesized that the transit time through the pre-B cell compartment or receptor editing may affect the extent of the cellular maturation defects in Btk-deficient B cells. To address this issue, we used 3-83μδ transgenic mice, which prematurely express a complete B cell receptor and therefore manifest accelerated B cell development. In Btk-deficient 3-83μδ mice, the IgM+ B cells in the bone marrow exhibited a very immature phenotype (pre-BCR+CD43+CD2−) and were arrested at the transitional type 1 B cell stage upon arrival in the spleen. However, these cellular maturation defects were largely restored when Btk-deficient 3-83μδ B cells were on a centrally deleting background and therefore targeted for receptor editing. Providing an extended time window for developing B cells by enforced expression of the antiapoptotic gene Bcl-2 did not alter the Btk dependence of their cellular maturation. We conclude that premature B cell receptor expression amplifies the cellular maturation defects in Btk-deficient B cells, while extensive receptor editing reduces these defects.

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“…Because xid mice can make convincing antibody responses to some TI antigens but not others, it has been convenient to view such antigens as being one of two types; TI-1 antigens that elicit an antibody response in xid mice, and TI-2 antigens that do not (5,11,13). It has been proposed that xid mice lack a subpopulation of B cells required for normal antibody responses to TI-2 antigens (reviewed in references 5 and 32).…”

Section: Discussionmentioning

confidence: 99%

Antibody response of immunodeficient (xid) CBA/N mice to Escherichia coli 0113 lipopolysaccharide, a thymus-independent antigen.

Hiernaux¹,

Jones²,

Rudbach³

et al. 1983

The Journal of Experimental Medicine

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CBA/N mice, which possess an X-linked immunodeficiency (xid), produce a convincing antibody response to lipopolysaccharide derived from Escherichia coli 0113 (LPS 0113), a thymus-independent antigen. The antibody response produced was shown to be specific for the O-polysaccharide moiety of LPS 0113, rather than lipid A or lipid-A-associated protein. The relevance of this finding to the nature of the genetic defect of xid-mice is discussed.

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CBA/N Immune Defective Mice; Evidence for the Failure of a B Cell Subpopulation to be Expressed

Cited by 113 publications

References 73 publications

Production of a B cell growth-promoting activity, (DL)BCGF, from a cloned T cell line and its assay on the BCL1 B cell tumor.

Production of a B cell growth-promoting activity, (DL)BCGF, from a cloned T cell line and its assay on the BCL1 B cell tumor.

Cellular Maturation Defects in Bruton’s Tyrosine Kinase-Deficient Immature B Cells Are Amplified by Premature B Cell Receptor Expression and Reduced by Receptor Editing

Antibody response of immunodeficient (xid) CBA/N mice to Escherichia coli 0113 lipopolysaccharide, a thymus-independent antigen.

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