Agammaglobulinæmia With B Lymphocytes Specific Defect of Plasma-Cell Differentiation

Cooper, M. D.; Lawton, Alexander R.; Bockman, DaleE.

doi:10.1016/s0140-6736(71)92742-5

Cited by 223 publications

(71 citation statements)

References 20 publications

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“…Similarly, individuals with IgA-D have normal numbers of IgA-bearing B cells, but these are relatively immature and fail to undergo terminal differentiation into IgA-secreting plasma cells (5). The arrests in B-cell differentiation seen in CVID and IgA-D are thus similar and contrast with the arrest seen at the pre-Bto B-cell stage in the X chromosome-linked form of congenital agammaglobulinemia (3,6).…”

Section: Common Variable Immunodeficiency (Cvid) and Selectivementioning

confidence: 99%

“…CVID, typically manifested by recurrent bacterial infections, is usually recognized in adolescents or young adults and thus is sometimes called the late-onset form of hypogammaglobulinemia. In most individuals with CVID, B cells are produced in normal numbers but they fail to undergo differentiation into antibody-secreting plasma cells (3,4). Similarly, individuals with IgA-D have normal numbers of IgA-bearing B cells, but these are relatively immature and fail to undergo terminal differentiation into IgA-secreting plasma cells (5).…”

Section: Common Variable Immunodeficiency (Cvid) and Selectivementioning

confidence: 99%

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Individuals with IgA deficiency and common variable immunodeficiency share polymorphisms of major histocompatibility complex class III genes.

Schaffer

Palermos

Zhu

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

147

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IgA deficiency and common variable immunodeficiency are heritable disorders that can occur within the same family. Both immunodeficiencies are characterized by arrests in B-cell differentiation that vary in the extent of the immunoglobulin isotypes involved. A high frequency of major histocompatibility complex supratypes associated with a null allele of the gene encoding the C4A isotype of complement component C4 has been observed in IgA-deficient individuals. In search of a genetic linkage between the two immunodeficiencies, we examined the major histocompatibility complex (MHC) class HI genes encoding complement components C2, C4A, and C4B and steroid 21-hydroxylase in addition to the HLA serotypes in individuals with either common variable immunodeficiency or IgA deficiency. Twelve of 19 patients with common variable immunodeficiency (63%, P < 0.001) and 9 of 16 patients with IgA deficiency (56%, P < 0.01) had rare C2 alleles and/or C4A and 21-hydroxylase A deletions, whereas these gene features were seen in only 5 of 34 healthy individuals (15%) in the control group. Nine of 11 patients with C4A deletion had an HLA haplotype consistent with the MHC

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Section: Common Variable Immunodeficiency (Cvid) and Selectivementioning

confidence: 99%

Section: Common Variable Immunodeficiency (Cvid) and Selectivementioning

confidence: 99%

Individuals with IgA deficiency and common variable immunodeficiency share polymorphisms of major histocompatibility complex class III genes.

Schaffer

Palermos

Zhu

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

147

View full text Add to dashboard Cite

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“…Recent developments in the field of cellular immunology have now permitted differentiations of different types of mononuclear cells (1)(2)(3)(4)(5)(6)(7). Human lymphocytes may be classified, based upon animal experiments and studies in patients with immunodeficiency states, into at least two groupsthymic-dependent lymphocytes (T cells) and thymicindependent or bone marrow-derived lymphocytes (B cells) (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13). T cells are thought to mediate reactions of cellular immunity, whereas B cells are primarily concerned with humoral immunity (14,15).…”

Section: Immunologic Characterization Of the Mononuclear Cell Infiltrmentioning

confidence: 99%

Immunologic characterization of the mononuclear cell infiltrates in rheumatoid synovia, in rheumatoid nodules, and in lip biopsies from patients with sjö;ugren's syndrome

Tannenbaum

Pinkus

Anderson

et al. 1975

Arthritis & Rheumatism

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Two subcutaneous rheumatoid nodules and 8 rheumatoid synovia from patients with rheumatoid arthritis (RA); and 2 parotid glands, 1 “pseudolymphoma,” and 6 lip biopsies from patients with Sjögren' syndrome (SS) were studied to identify mononuclear cells. The palisading mononuclear cells in subcutaneous nodules had a surface membrane receptor for complement. B lymphocytes surrounded by larger numbers of non‐B lymphocytes were found in RA synovium and between salivary ducts of SS lip biopsies. A “pseudolymphoma” obtained from a patient with SS consisted primarily of B lymphocytes. The predominant mononuclear cells in rheumatoid synovia and salivary glands in patients with RA and SS do not have surface membrane receptors for complement and are thus probably T lymphocytes or null cells.

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“…Differential expression of cellsurface immunoglobulin or THY1 (also known as CD90) by B cells and T cells, respectively, was shown in mice in 1970 (REF. 46) and the next year, the cell-surface expression of immunoglobulins was shown to be restricted to B cells in chickens and humans [47][48][49] .…”

Section: Implications Of B Cell and T Cell Lineagesmentioning

confidence: 99%

The early history of B cells

2015

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Agammaglobulinæmia With B Lymphocytes Specific Defect of Plasma-Cell Differentiation

Cited by 223 publications

References 20 publications

Individuals with IgA deficiency and common variable immunodeficiency share polymorphisms of major histocompatibility complex class III genes.

Individuals with IgA deficiency and common variable immunodeficiency share polymorphisms of major histocompatibility complex class III genes.

Immunologic characterization of the mononuclear cell infiltrates in rheumatoid synovia, in rheumatoid nodules, and in lip biopsies from patients with sjö;ugren's syndrome

The early history of B cells

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