Altered idiotype response to phosphocholine in mice bearing an x-linked immune defect

• Published in: The Journal of immunology (1950) Vol. 127; no. 4; pp. 1629 - 1633
• Main Authors: Kenny, JJ, Guelde, G, Claflin, JL, Scher, I
• Format: Journal Article
• Language: English
• Published: United States Am Assoc Immnol 01.10.1981
• Subjects: Animals; Cell Separation; Choline - analogs & derivatives; Female; Flow Cytometry; Immunoglobulin Idiotypes - biosynthesis; Immunoglobulin Idiotypes - genetics; Immunoglobulin Idiotypes - immunology; Immunoglobulin M - biosynthesis; Immunologic Deficiency Syndromes - genetics; Immunologic Deficiency Syndromes - immunology; Isoelectric Focusing; Male; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Inbred CBA; Phosphorylcholine - immunology; Sex Chromosomes - immunology; Spleen - immunology; X Chromosome - immunology
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.127.4.1629

The x-linked CBA/N defect results in an altered idiotype expression among the anti-phosphocholine (PC) antibodies produced after antigenic challenge with the thymic dependent antigen PC-KLH but does not preclude the response to this hapten as previously suggested. The majority of immune-defective F1 male mice can be divided into 2 groups based on their T15 idiotype profile. Group 1 mice fail to produce anti-PC antibodies bearing the T15 idiotype in either a primary or secondary response, whereas group 2 mice produce low levels of T15 idiotype; however, this idiotype often appears only after secondary immunization. These responses are distinct from the anti-PC response of normal F1 females, which is predominantly of the T15 idiotype. In addition to the altered idiotype expression, F1 male mice exhibited a greatly reduced primary anti-PC response compared to normal mice, and secondary responses were approximately one-third that of normal mice. The delayed expression of anti-PC antibodies in immune defective mice appears to be due to their inability to produce IgM anti-PC antibodies in either a primary or secondary response to PC-KLH.