IMMUNOGLOBULINS Immunoglobulin Classes I Ig G u u

IMMUNOGLOBULINS

Immunoglobulin Classes I. Ig. G u u u Structure: Monomer (m. wt 150, 000) Percentage serum antibodies: 75 -80% Is the major Ig in extra vascular spaces Location: Blood, lymph, intestine Half-life in serum: 23 days Complement Fixation: Yes (Ig. G 4 does complement. ) not fix u Placental Transfer: Yes u Known Functions: is the most versatile immunoglobulin, because it is capable of carrying out all of the functions of IG molecules: • Enhances phagocytosis • Neutralizes toxins and viruses, • Protects fetus and newborn.

Ig. G

II. Ig. M u Structure: Pentamer (m. wt 900, 000) u Has an extra domain on the μ chain (CH 4) & it has another protein covalently bound via an S-S bond called the J chain, This chain functions in polymerization of the molecule into a pentamer u Percentage serum antibodies: 5 -10% u Location: Blood, lymph u Half-life in serum: 5 days u Complement Fixation: Yes u Placental Transfer: No u Known Functions: • First antibodies produced during an infection. • Effective against microbes and agglutinating antigens.

III. Ig. A u Structure: Dimer (m. wt 150, 000 -350, 000) u When Ig. A exits as a dimer, a J chain is associated with it. u Percentage serum antibodies: 10 -15% u Location: Secretions (tears, saliva, intestine, milk), blood and lymph. u Half-life in serum: 6 days u Complement Fixation: Normally does not fix complement, unless aggregated. u Placental Transfer: No u Known Functions: • Localized protection of mucosal surfaces. • Provides immunity to infant digestive tract.

IV. Ig. D u u u u Structure: Monomer (m. wt 180, 000) Percentage serum antibodies: 0. 2% Location: B-cell surface, blood, and lymph Half-life in serum: 3 days Complement Fixation: No Placental Transfer: No Known Functions: In serum function is unknown. On B cell surface, initiate immune response.

V. Ig. E u Structure: Monomer(m. wt 190, 000) u Percentage serum antibodies: 0. 002% u Ig. E is the least common serum Ig since it binds very tightly to Fc receptors on basophils & Mast cells even before interacting with Ag. u Location: Bound to mast cells and basophils throughout body. u Half-life in serum: 2 days u Complement Fixation: No u Placental Transfer: No u Known Functions: Allergic reactions. Possibly lysis of worms.

CLINICAL IMPLICATIONS OF HUMAN IMMUNOGLOBULIN CLASSES Ig. G Increases in: 1) Chronic granulomatous infections. 2) Infections of all types. 3) Hyperimmunization. 4) Liver disease. 5) Severe Malnutrition. 6) Dysproteinemia. 7) Rheumatoid arthritis. Decreases in: 1) Agammaglobulinemia. 2) Lymphoid aplasia. 3) Selective Ig. G & Ig. A deficiency 4) Ig. A myeloma. 5) Bence Jones proteinemia. 6) Chronic lymphocytic leukemia.

Ig. M increases (in newborns) - A level of Ig. M above 20 mg/dl is an indication of in utero infection: 1)- rubella virus. 2)- cytomegalovirus. 3)- syphilis. 4)- toxoplasmosis. Ig. M increases (in adults) in: 1) Waldenström’s macroglobulinemia. 2) Trypanosomiasis. 3) Actinomycosis. 4) Malaria 5)Infectious mononucleosis. 6) Lupus erythematosus. 7) Rheumatoid arthritis. Ig. M decreases in: 1) Agammaglobulinemia. 2). Lymphoid aplasia. 3) Ig. G & Ig. A myeloma. 4) Dysgammaglobulinemia. 5) Chronic lymphocytic leukemia.

Ig. A increases in: 1) Wiskott-Aldrich syndrome. 2) Most cases of liver Cirrhosis 3) Certain stages of collagen & other autoimmune disorders such as rheumatoid arthritis & lupus erythematosus. 4) Ig. A myeloma. Ig. A decreases in: 1) Hereditary ataxia telangiectasia. 2) Immunologic deficiency states (e. g. : dysgammaglobulinemi a, congenital & acquired agammaglobulinemia, & hypogammaglobulinemia). 3) Malabsorption syndromes. 4) Lymphoid aplasia. 5) Ig. G myeloma. 6) Acute & Chronic lymphoblastic leukemia.

Ig. D increases in: 1) Chronic infections. 2) Ig. D myelomas. Ig. E increases in: 1) Atopic skin diseases such as eczema. 2) Hay fever. 3) Asthma. 4) Anaphylactic shock. 5) Ig. E-myeloma. Ig. E decreases in: - Congenital agammaglobulinemia

Immunoglobulin Structure Disulfide bond Carbohydrate CL VL CH 2 CH 1 VH Hinge Region CH 3