Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2010-4-7
pubmed:abstractText
Abnormalities in humoral immunity typically reflect a generalized or selective failure of effective B-cell development. The developmental processes can be followed through analysis of cell-surface markers, such as IgM, IgD, CD10, CD19, CD20, CD21, and CD38. Early phases of B-cell development are devoted to the creation of immunoglobulin and testing of B-cell antigen receptor signaling. Failure leads to the absence of B cells and immunoglobulin in the blood from birth. As the developing B cells begin to express a surface B-cell receptor, they become subject to negative and positive selection pressures and increasingly depend on survival signals. Defective signaling can lead to selective or generalized hypogammaglobulinemia, even in the presence of normal numbers of B cells. In the secondary lymphoid organs some B cells enter the splenic marginal zone, where preactivated cells lie ready to rapidly respond to T-independent antigens, such as the polysaccharides that coat some microorganisms. Other cells enter the follicle and, with the aid of cognate follicular T cells, divide to help form a germinal center (GC) after their interaction with antigen. In the GC B cells can undergo the processes of class switching and somatic hypermutation. Failure to properly receive T-cell signals can lead to hyper-IgM syndrome. B cells that leave the GC can develop into memory B cells, short-lived plasma cells, or long-lived plasma cells. The latter ultimately migrate back to the bone marrow, where they can continue to produce protective antigen-specific antibodies for decades.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1097-6825
pubmed:author
pubmed:copyrightInfo
Copyright (c) 2010 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
125
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
778-87
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Clinical consequences of defects in B-cell development.
pubmed:affiliation
Division of Clinical Immunology and Rheumatology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Ala, USA.
pubmed:publicationType
Journal Article, Review, Research Support, N.I.H., Extramural