Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0348321 (Haemophilus)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antibody response to the capsular polysaccharide of Haemophilus influenzae type b was evaluated after vaccination with the capsular polysaccharide or its tetanus toxoid conjugate in 41 randomized patients with recurrent infections, IgA deficiency, common variable immunodeficiency, or the Wiskott-Aldrich syndrome. Serum antibodies were measured using a Farr assay for total antibodies and an enzyme-linked immunosorbent assay for antibodies of the three main immunoglobulin classes and of each IgG subclass. Antibody levels reached concentrations generally considered as protective in the majority of cases, the best response being observed after two injections of the conjugate vaccine with a 1-month interval. Vaccination with the conjugate therefore seems to be promising for the prevention of Haemophilus influenzae type b infections in such patients.
 ...
PMID:Immunogenicity of Haemophilus influenzae type b capsular polysaccharide and its tetanus toxoid conjugate in patients with recurrent infections or humoral immunodeficiency. 159 74

Antibodies directed to capsular polysaccharides form an essential component in the defence against infections with encapsulated bacteria such as Streptococcus pneumoniae and Haemophilus influenzae type b. Immune responses to polysaccharide antigens can occur in the absence of a functional thymus and the antigens are therefore designated as thymus independent. However, regulatory T cells may influence the magnitude of the antibody response to capsular polysaccharide antigens. So-called thymus independent type 2 antigens share several features of their immune response such as late development of antibody synthesis in ontogeny, no memory formation and a restricted isotype (IgM, IgG2) and idiotype usage. In infants and young children up to the age of 2 years the antibody response to capsular polysaccharides is inadequate resulting in an increased incidence of diseases such as pneumonia, meningitis, otitis and other forms of bacteremic disease. Anti-capsular polysaccharide antibody deficiency does occur in a number of well defined immunodeficiency syndromes including hypo- or agammaglobulinaemia, selective IgA and/or IgG subclass deficiency, Wiskott-Aldrich syndrome, DiGeorge anomaly and also in acquired immune deficiencies such as AIDS, and some forms of lymphoid malignancies. In elderly and in conditions such as splenectomy an increased incidence of infections with encapsulated bacteria does occur, sometimes but not always on basis of a defect in antibody formation. Clinicians are often confronted with young patients older than 2 years of age suffering from recurrent severe bacterial infections of the respiratory tract. In these patients no overt immunodeficiency is demonstrable but recent results indicated that a small percentage may show a selective defect in the antibody response since upon vaccination with polysaccharide vaccines no increase in antibody titer does occur. Though antibodies to polysaccharide antigens in young children are mainly of the IgM and IgG1 (IgG3) isotype, in older children and adults the polysaccharide antibodies are predominantly localized in the IgG2 subclass. The bridge between IgG2 type antibodies and phagocytosis of encapsulated bacteria is constituted by Fc gamma receptors for IgG2 on effector cells. The recent finding that allotypes of Fc gamma RIIa do exist that either bind or do not bind IgG2 type antibodies strongly suggests that the defence of a given individual to encapsulated bacteria apart from an intact antibody formation and the complement system also is determined by the allotype of the appropriate Fc gamma receptor.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Anti-capsular polysaccharide antibody deficiency states. 816 45

Primary immune deficiencies (PIDs) are characterized by functional and/or quantitative abnormalities of one or more immune system components. Several bone and joint abnormalities can occur in patients with PID, with arthritis being the most common. Joint manifestations, of which arthritis is the most common, occur chiefly in humoral PIDs (agammaglobulinemia, common variable immunodeficiency, hyper-IgM syndromes, and IgA deficiency) and occasionally in other PIDs (chronic granulomatous disease and Wiskott-Aldrich syndrome). Monoarthritis or oligoarthritis is the usual pattern, although polyarthritis may occur, occasionally with nodules suggesting rheumatoid arthritis. Arthritis in patients with PID is usually infectious in nature, the most common causative organism being Mycoplasma, followed by Staphylococcus, Streptococcus, and Haemophilus. These bacteria can induce not only synovial infections, but also aseptic arthritogenic inflammatory responses. Arthritis having no demonstrable relation to chronic infection has been reported also and ascribed to dysimmunity-driven mechanisms that exhibit a number of specific features. Bone lesions are far less common and usually due to infections complicating humoral PID. Distinctive bone manifestations occur in a number of rare PIDs (e.g., hyper-IgE syndrome and Di George syndrome) and in syndromes characterized by spondyloepiphyseal dysplasia. Familiarity with PID syndromes both enhances the diagnostic capabilities of physicians and provides insight into the pathophysiology of bone and joint abnormalities associated with immune dysfunction. In children and occasionally in adults, a combination of bone and/or joint manifestations and hypogammaglobulinemia may indicate PID. When there is no evidence of lymphoproliferative disease, infection, or iatrogenic complications, investigations for PID should be obtained. PID-related arthritis is a unique model for studying the pathogenesis of presumably postinfectious arthritis and of inflammatory joint diseases including rheumatoid arthritis.
 ...
PMID:Bone and joint disease associated with primary immune deficiencies. 1637 4