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Comparative studies on cell-mediated immunity in patients with different warts
Dermatologica
|January 1, 1980
Summary
Cell-mediated immunity (CMI) is impaired in various wart types, most severely in flat warts and epidermodysplasia verruciformis (EV). This suggests human papillomavirus (HPV) type influences infectivity and host resistance.
Area of Science:
- Immunology
- Dermatology
- Virology
Background:
- Warts are common skin lesions caused by human papillomavirus (HPV) infections.
- Cell-mediated immunity (CMI) plays a crucial role in controlling HPV infections.
- The extent of CMI impairment may vary with different clinical forms of warts.
Purpose of the Study:
- To investigate CMI in patients with diverse wart types and epidermodysplasia verruciformis (EV).
- To correlate CMI status with specific clinical manifestations of HPV infection.
- To explore the role of HPV type in disease pathogenesis and host resistance.
Main Methods:
- Assessed peripheral blood T and B lymphocyte distribution.
- Measured in vitro lymphocyte response to phytohemagglutinin (PHA).
- Evaluated in vivo DNCB sensitization and T cell rosette formation.
Main Results:
- Significantly decreased T lymphocytes forming E rosettes in common, flat, plantar warts, and EV compared to controls.
- Reduced DNCB sensitivity and PHA response observed across most patient groups, indicating CMI defects.
- Most pronounced T cell dysfunction noted in EV and flat wart patients; common warts showed a slight defect. Plantar and genital warts exhibited near-normal CMI.
- CMI defects varied significantly among different wart types, suggesting HPV type-specific infectivity and host resistance.
Conclusions:
- CMI defects are divergent across various clinical forms of HPV-induced warts.
- Specific HPV types may differ in their infectivity and ability to evade host immune responses.
- Host cell-mediated resistance is a fundamental factor in preventing and controlling HPV infections.