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Immunological evaluation of late complement component-deficient individuals.
A E Platonov1, V B Beloborodov, D I Gabrilovitch
1Central Institute of Epidemiology, Moscow, Russia.
Clinical Immunology and Immunopathology
|August 1, 1992
Summary
Late complement component deficiency may impair neutrophil activation, increasing susceptibility to meningococcal disease. Further research is needed to understand the role of terminal complement components in immune response.
Area of Science:
- Immunology
- Complement System
- Infectious Disease
Background:
- Late complement component deficiencies are linked to increased susceptibility to Neisseria meningitidis infections.
- Previous studies have not systematically investigated additional immunologic factors contributing to this susceptibility.
Purpose of the Study:
- To examine immunologic variables in individuals with late complement component deficiency and a history of meningococcal infection.
- To compare these variables with those in healthy individuals and complement-sufficient individuals with recurrent meningitis.
Main Methods:
- Studied three groups: healthy individuals, complement-sufficient individuals with recurrent meningitis, and complement-deficient individuals with prior meningococcal infection.
- Analyzed lymphocyte subsets (CD3+, CD4+, CD8+, CD20+, CD16+), CD4+/CD8+ ratio, C4, circulating immune complexes, and immunoglobulin (IgG, IgM, IgA) concentrations.
- Assessed neutrophil activation coefficients (spontaneous and lipopolysaccharide-stimulated).
Main Results:
- No significant differences in lymphocyte counts, subsets, CD4+/CD8+ ratio, C4, or immune complexes among groups.
- Slightly decreased IgG, IgM, and IgA concentrations were observed in complement-deficient individuals.
- Significantly depressed spontaneous and stimulated neutrophil activation was noted in complement-deficient individuals.
Conclusions:
- Terminal complement components may be crucial for optimal neutrophil activation.
- Impaired neutrophil activation in complement deficiency could contribute to increased susceptibility to meningococcal disease.