- T-Cell
- Impaired Development (SCID, Digeorges syndrome)
- Impaired Maturation, Functioning
- SCID,
- Hyper-IgE or JOBS syndrome (STAT3 mutation)
- Wiskott-Aldrich, Ataxia-Telangiectasia)
- Mechanism of T-cell mediated Immune system
- Th1 (interferon-γ–producing lymphocytes and IL 12)
- Control Intracellular Infection
- Th2 (interleukin-4–producing lymphocytes and TGF B)
- Direct antibody-mediated protection against extracellular infection
- Hyper Ig E syndrome
- Th17 -
- In response of infection (like yeastB-glucan binding to dectin-1) transforms CD4+ T cell to Th17 by a STAT 3 dependent process
- Th17 cell procudes IL -22 and IL-17. Together, IL-22 and IL-17 work to generate DEFENSINS in the epithelial tissue
- STAT 3 mutation can lead to the defective interaction causing decreased production of DEFENSINS
- Defect in Leucocyte activation in the epithelium mediated through IL-17 leads to mucocutaneous infection
J Allergy Clin Immunol 2010;125:S33-40.
B cell differentiation and related primary immunodeficiencies (PIDs) Harrison's Principles of Internal Medicine, 19e
Selective Antibody Deficiency
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