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Concept
T cell deficiency
Résumé
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. 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).
Presentations differ among causes, but T cell insufficiency generally manifests as unusually severe common viral infections (respiratory syncytial virus, rotavirus), diarrhea, and eczematous or erythrodermatous rashes. Failure to thrive and cachexia are later signs of a T-cell deficiency.
In terms of the normal mechanism of T cell we find that it is a type of white blood cell that has an important role in immunity, and is made from thymocytes. One sees in the partial disorder of T cells that happen due to cell signaling defects, are usually caused by hypomorphic gene defects. Generally, (micro)deletion of 22Q11.2 is the most often seen.
The main pathogens of concern in T cell deficiencies are intracellular pathogens, including Herpes simplex virus, Mycobacterium and Listeria. Also, intracellular fungal infections are also more common and severe in T cell deficiencies. Other intracellular pathogens of major concern in T cell deficiency are:
The diagnosis of T cell deficiency can be ascertained in those individuals with this condition via the following:
Delayed hypersensitivity skin test
T cell count
Detection via culture(infection)
Primary (or hereditary) immunodeficiencies of T cells include some that cause complete insufficiency of T cells, such as severe combined immunodeficiency (SCID), Omenn syndrome, and Cartilage–hair hypoplasia.
Secondary causes are more common than primary ones. Secondary (or acquired) causes are mainly:
AIDS
Cancer chemotherapy
Lymphoma
Glucocorticoid therapy
Complete insufficiency of T cell function can result from hereditary conditions (also called primary conditions) such as severe combined immunodeficiency (SCID), Omenn syndrome, and cartilage–hair hypoplasia.
Source officielle
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