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The defect in the immunoglobulins presumably arises during somatic hypermutation.
Mistargeted somatic hypermutation is a likely mechanism in the development of B-cell lymphomas.
These cells normally engulf B cells that have undergone apoptosis after somatic hypermutation.
The protein is involved in somatic hypermutation, gene conversion, and class-switch recombination of immunoglobulin genes.
Autoreactive B cells can accidentally emerge during somatic hypermutation and migrate into the germinal center light zone.
Somatic hypermutation involves a programmed process of mutation affecting the variable regions of immunoglobulin genes.
He demonstrated the importance of somatic hypermutation of immunoglobulin V genes in antibody affinity maturation.
Although the exact mechanism of the somatic hypermutation is still not known, a major role for the Activation-Induced (Cytidine) Deaminase has been discussed.
Somatic hypermutation (or SHM) is a cellular mechanism by which the immune system adapts to the new foreign elements that confront it (for example, microbes).
Since B cell maturation also involves somatic hypermutation (a process completed before differentiation into a plasma cell), these antibodies frequently have a very high affinity for their antigen.
This is unfortunate because somatic hypermutation does give rise to clones capable of producing soluble antibodies that would have bound the altered epitope avidly enough to neutralize it.
Targets: M-protein levels in blood, patient-specific assays for immunoglobulin and T cell receptor genes (high levels of somatic hypermutation often prevent this assay from reliably working).
B-cells within the germinal center proliferate and undergo immunoglobulin somatic hypermutation (SHM) of IgV region genes to revise their antigen receptors.
For example, the vertebrate immune system shows that the variable environment of antigens has provided selective pressure for the use of adaptable codons and low-fidelity polymerases during somatic hypermutation.
Interleukin 4 (IL4) is produced by CD4 T cells specialized in providing help to B cells to proliferate and to undergo class switch recombination and somatic hypermutation.
His theory predicted almost all of the key features of the immune system as we understand it today, including autoimmune disease, immune tolerance and somatic hypermutation as a mechanism in antibody production.
In these rapidly dividing cells, the genes encoding the variable domains of the heavy and light chains undergo a high rate of point mutation, by a process called somatic hypermutation (SHM).
B-1 B cells sequences also show no evidence for somatic hypermutation (SHM), and few non-templated nucleotide (N) sequence insertions, a pattern typical of neonatal B cells.
After several days of expansion the B cells undergo somatic hypermutation, a process by which they mutate their antibody-encoding DNA and thus generate a diversity of clones in the germinal center.
Other AID/APOBEC family members are involved in mRNA editing, somatic hypermutation and recombination of immunoglobulin genes, and innate immunity to retroviral infection.
AID (AICDA) expression causes B cell antibodies to class switch from IgM/IgD to other antibody isotopes and drives somatic hypermutation during clonal proliferation.
Also, apoptotic chromatin and nuclei may attach to the surfaces of follicular dendritic cells and make this material available for activating other B cells that may have randomly acquired self-specificity through somatic hypermutation.
These algorithms focus on the Darwinian attributes of the theory where selection is inspired by the affinity of antigen-antibody interactions, reproduction is inspired by cell division, and variation is inspired by somatic hypermutation.
Additional diversity is attained by junctional diversity, resulting from the random additional of nucleotides by terminal deoxynucleotidyltransferase, and by somatic hypermutation, which occurs during B cell maturation in the spleen and lymph nodes.
Hyper-IgM syndrome type 4 is a form of Hyper IgM syndrome which is a defect in class switch recombination downstream of the AICDA gene that does not impair somatic hypermutation.