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B cell mitogen 95 B lymphocyte<br />

infectious mononucleosis or a proliferating and relentless<br />

lymphoma that produces high mortality. Monoclonal antibodies<br />

to the B cell antigens, CD21 and CD24, have proven<br />

effective in controlling the B cell proliferation, but further<br />

studies are needed.<br />

B cell mitogen<br />

Substance that induces B cell division and proliferation.<br />

B cell receptor (BCR) complex<br />

The antigen receptors of B cells, each of which makes a<br />

single type of immunoglobulin. The form of this immunoglobulin<br />

on the cell surface is the B cell receptor for<br />

the antigen of interest in addition to the membranebound<br />

immunoglobulin monomers of the intracellular<br />

signaling molecules that comprise the accessory Igα/Igβ<br />

complex.<br />

B cell-specific activator protein (BSAP)<br />

A transcription factor that has an essential role in early<br />

and later stages of B cell development. It is encoded by the<br />

gene Pax-5.<br />

B cell-stimulating factor 1 (BSF-1)<br />

An earlier term for interleukin-4.<br />

B cell-stimulating factor 2 (BSF-2)<br />

An earlier term for interleukin-6.<br />

B cell tolerance<br />

B cell tolerance is manifested as a decreased number of<br />

antibody-secreting cells following antigenic stimulation,<br />

compared to a normal response. Hapten-specific tolerance<br />

can be induced by inoculation of deaggregated haptenated<br />

γ-globulins (Ig). Induction of tolerance requires membrane<br />

Ig cross-linking. Tolerance may have a duration of 2 months<br />

in B cells of the bone marrow and 6 to 8 months in T cells.<br />

Whereas prostaglandin E (PGE) enhances tolerance induction,<br />

interleukin-1 (IL-1), lipopolysaccharide (LPS), and<br />

8-bromoguanosine block tolerance instead of an immunogenic<br />

signal. Tolerant mice carry a normal complement<br />

of hapten-specific B cells. Tolerance is not attributable to<br />

a diminished number or isotype of antigen receptors. It<br />

has also been shown that the six normal activation events<br />

related to membrane Ig turnover and expression do not<br />

occur in tolerant B cells. Although tolerant B cells possess a<br />

limited capacity to proliferate, they fail to do so in response<br />

to antigen. Antigenic challenge of tolerant B cells induces<br />

them to enlarge and increase expression, yet they are apparently<br />

deficient in a physiologic signal requisite for progression<br />

into a proliferative stage.<br />

B cell tyrosine kinase (Btk)<br />

Src family tyrosine kinase that plays a critical role in the<br />

maturation of B lymphocytes. Btk gene mutations lead to<br />

X-linked agammaglobulinemia in which B cell maturation<br />

is halted at the pre-B stage.<br />

B cells<br />

The B lymphocytes that derive from the fetal liver in the<br />

early embryonal stages of development and from the bone<br />

marrow thereafter. In birds, maturation takes place in the<br />

bursa of Fabricius, a lymphoid structure derived from an<br />

outpouching of the hindgut near the cloaca. In mammals,<br />

maturation is in the bone marrow. Plasma cells that synthesize<br />

antibody develop from precursor B cells.<br />

B complex<br />

The major histocompatibility complex (MHC) in chickens.<br />

Genes at these loci determine MHC class I and II antigens<br />

and erythrocyte antigens.<br />

9–12µm<br />

B cell.<br />

B genes<br />

Situated within the major histocompatibility complex<br />

(MHC) locus on the short arm of chromosome 6, they are<br />

called MHC class III genes. TNF-α and TNF-β genes are<br />

situated between the C2 and HLA-B genes. Another gene<br />

designated FD lies between the Bf and C4a genes. C2 and<br />

B complete primary structures have been deduced from<br />

cDNA and protein sequences. C2 is comprised of 732<br />

residues and is an 81-kDa molecule, whereas B contains 739<br />

residues and is a 83-kDa molecule. Both proteins have three<br />

domains. Certain HLA alleles occur at a higher frequency<br />

in individuals with particular diseases than in the general<br />

population. This type of data permits estimation of the relative<br />

risk (RR) of developing a disease for every known HLA<br />

allele. For example, there is a strong association between<br />

ankylosing spondylitis, an autoimmune disorder involving<br />

the vertebral joints, and the major histocompatibility<br />

complex (MHC) class I allele, HLA-B27. There is a strong<br />

association between products of the polymorphic class II<br />

alleles HLA-DR and DQ and certain autoimmune diseases,<br />

as MHC class II molecules are of great importance<br />

in the selection and activation of CD4 + T lymphocytes that<br />

regulate immune responses against protein antigens. For<br />

example, 95% of Caucasians with insulin-dependent (type<br />

I) diabetes mellitus have HLA-DR3, HLA-DR4, or both.<br />

There is also a strong association of HLA-DR4 with rheumatoid<br />

arthritis. Numerous other examples exist and are<br />

the targets of current investigations, especially in extended<br />

studies employing DNA probes. Methods of calculating the<br />

RR and absolute risk (AR) can be found under definitions<br />

for those terms.<br />

B locus<br />

The major histocompatibility locus in the chicken.<br />

B lymphocyte<br />

Lymphocytes of the B cell lineage that mature under the<br />

influence of the bursa of Fabricius in birds and in the bursa<br />

equivalent (bone marrow) in mammals. B cells occupy follicular<br />

areas in lymphoid tissues and account for 5 to 25% of<br />

all human blood lymphocytes that number 1000 to 2000 cells<br />

per mm 3 . They comprise most of the bone marrow lymphocytes,<br />

one third to one half of the lymph node and spleen<br />

lymphocytes sites, but less than 1% of those in the thymus.<br />

Nonactivated B cells circulate through the lymph nodes and<br />

the spleen. They are concentrated in follicles and marginal<br />

zones around the follicles. Circulating B cells may interact<br />

B

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