Purpose of review: Host defense against community-acquired pneumonia depends on an intact innate and acquired immune system. This review analyses the correlation between specific defects and polymorphisms of immunity genes with susceptibility for pneumonia.
Recent findings: Mutations in BTK, Bruton's tyrosine kinase, lead to X-linked agammaglobulinemia, a disease characterized by recurrent respiratory tract infections, including pneumonia. BTK inhibitors, which are used for treatment of leukemia, have pneumonia as side effect. Polymorphisms in B lymphocyte growth and differentiation factors, including IL-6 and IL-10, Fcg RIIa receptors, as well as genetic variants of ACE, angiotensin-converting enzyme, also are associated with increased susceptibility for pneumonia.
Summary: Delineation of underlying genetic defects and polymorphisms may add in diagnosis, therapy, and prognosis of community-acquired pneumonia. In case of humoral immunodeficiency, antibody replacement therapy may be indicated.