A formula to assess lymphocyte responsiveness in vitro.
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We determined the B cell subpopulations that produce the major cross-reactive idiotype (CRIA) associated with the anti-phenylarsonate (ARS) antibody response of A/J mice. Specifically, we examined the B2 subpopulation found in normal mice which, in H-2b mice, bears the I-Ab-encoded determinant Ia.W39; the B1 subpopulation found in mice expressing the CBA/N X-linked immunodeficiency trait (xid); and the B1 subpopulation found in normal mice after the cytotoxic elimination of B2 cells with anti-Ia. W39 and complement. CRIA is expressed in each of these B cell subpopulations. Antigen plays a selective role in the stimulation of distinct B cell sets. ARS conjugates of keyhole limpet hemocyanin (KLH) can activate both the B1 and B2 subpopulations. In contrast, ARS conjugates of synthetic polypeptides under Ir gene control selectively activate the B2 subpopulation in strains that are genetic responders to the carrier. This leads to the establishment of CRIA dominance where CRIA+ anti-ARS antibody is 70 to 95% of the total anti-arsonate antibody response. This class of antigens fails to activate the B1 cells in either normal or xid mice. We compared the CRIA+ antibody produced by selectively activated B2 cells to that produced by the B1 subpopulation in xid mice. For these comparisons, we used competitive radioimmunoassays that employed polyspecific anti-CRIA antiserum or monoclonal anti-CRIA antibodies specific for distinct idiotopes on the heavy chain of CRIA+ antibody. B2 cells produce a CRIA+ anti-ARS antibody that is idiotopically uniform among individual mice, and that closely approximates the hybridoma protein 36-65 (the heavy chain of 36-65 represents the germ line-encoded sequence of the unique CRIA structural gene (25]. In contrast, the CRIA+ antibody produced by the B1 cell subset of xid mice is idiotopically diverse among individual mice, and differs markedly from the 36-65 hybridoma protein. The extent of diversification found in CRIA+ antibody depends on the B cell subpopulation that produces it.
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Although serious morbidity from gastric restriction for morbid obesity is rare, outflow tract dilation after gastroplasty has become a well-recognized complication, and reoperation to decrease outflow tract size has become increasingly common. We report the case of a patient who developed outflow tract obstruction with subsequent malnutrition, recurrent infections, and marrow suppression. Extensive immunologic evaluation revealed impaired cutaneous reactivity to a battery of recall antigens. Other in vitro T cell functions, B cell functions, neutrophil respiration, and quantification of complements were within normal limits. The patient's immunodeficiency was attributed to protein-calorie malnutrition and was corrected with total parenteral nutrition. Recovery of immune function with renutriture was demonstrated, and coincident resolution of infection and marrow suppression also occurred. Because of the reversibility of the immunologic abnormality with appropriate nutritional therapy, it is important to consider and treat malnourishment in connection with any operation in which oral intake is severely limited.
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Although bone and joint infections do not seem to be more frequent in patients with immune deficiences than in normal subjects, it seems paradoxically that an immune deficiency is relatively frequent during fully diagnosed bone and joint infections: the discrepancy between the two types of data is not easy to explain. Serology and immunology laboratories give little information in the etiological diagnosis of bone and joint infections, with the exception of perhaps gonococcal infections (search for anti-gonococcal antibodies by immunofluorescence), staphylococcal infections (pasteurella, yersinia, tularemia and brucella infections). In most cases, although the abnormalities observed are due to infection of the organism by the germ, they have nothing characteristic of the bone and joint localisation itself.
The evaluation of suspected humoral immunodeficiency includes quantitative immunoglobulin levels and specific antibody assays. The Schick test is a simple procedure for measurement of specific diphtheria antibodies that has been overlooked because the availability of Schick test materials has been limited in recent years. We assessed the efficacy of the Schick test in screening for antibody deficiency states in 23 children. Five had positive Schick test reactions. All five had clinical and immunologic findings consistent with a primary immunodeficiency disorder. Each of these patients had at least one other abnormality of antibody formation detected. The Schick test is a simple screening device helpful in the assessment of immunocompetence.
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