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IRF4 is a transcription factor belonging to the Interferon Regulatory Factor (IRF) family of transcription factors. [8] [9] In contrast to some other IRF family members, IRF4 expression is not initiated by interferons; rather, IRF4 expression is promoted by a variety of bioactive stimuli, including antigen receptor engagement, lipopolysaccharide (LPS), IL-4, and CD40.
Interferon regulatory factors (IRF) are proteins which regulate transcription of interferons (see regulation of gene expression). [1] Interferon regulatory factors contain a conserved N-terminal region of about 120 amino acids , which folds into a structure that binds specifically to the IRF-element (IRF-E) motifs, which is located upstream of ...
Humoral immune deficiency (including B cell deficiency or dysfunction), with signs or symptoms depending on the cause, but generally include signs of hypogammaglobulinemia (decrease of one or more types of antibodies) with presentations including repeated mild respiratory infections, and/or agammaglobulinemia (lack of all or most antibody production) which results in frequent severe infections ...
PRDM1/BLIMP-1 is a master transcription factor regulating downstream cytokines. It is activated by TLRs and IRF-4, and is crucial in T cell, B cell, and myeloid lineage cell differentiations.
Hypogammaglobulinemia is an immune system disorder in which not enough gamma globulins are produced in the blood (thus hypo-+ gamma + globulin + -emia).This results in a lower antibody count, which impairs the immune system, increasing risk of infection.
T cell deficiency is a deficiency of T cells, caused by decreased function of individual T cells, it causes an immunodeficiency of cell-mediated immunity. [1] T cells normal function is to help with the human body's immunity, they are one of the two primary types of lymphocytes (the other being B cells ).
LECT2 Amyloidosis (ALECT2) is a form of amyloidosis caused by the LECT2 protein. It was found to be the third most common (~3% of total) cause of amyloidosis in a set of more than 4,000 individuals studied at the Mayo Clinic; the first and second most common forms the disorder were AL amyloidosis and AA amyloidosis, respectively.
This treatment alone is not wholly effective, and many people still experience other symptoms such as lung disease and noninfectious inflammatory symptoms. This treatment replenishes Ig subtypes that the person lacks, is given at frequent intervals for life, and is thought to help reduce bacterial infections and boost immune function. [ 25 ]