Laboratory Evidence for Impaired Cellular Immunity in Different Stages of Syphilis

Abstract

Abundant evidence suggests that Treponema pallidum (T.p.) escapes humoral immune defence despite the host produces antibodies early in the infection. Since the serologic responses in syphilis have been studied in detail this paper focuses on the cellular immune mechanisms. For this purpose the leukocyte migration inhibition was investigated in 17 patients in different stages of syphilis. Leukocyte migration inhibition assay was performed before, and 7 days, 3 weeks, 2 mo. and 1 yr after start of treatment. Ultrasonicated T.p. were used as antigen corresponding to 5 X 10(6) to 2 X 10(7) Treponema pallida per ml. Controls without antigen, with addition of Concanavalin. A instead of T.p. and using cells of normal volunteers were run. There was no leukocyte migration inhibition before treatment, suggesting nonexistent or depressed cellular immunity in the untreated syphilitic patient. Significant leukocyte migration inhibition, however, was observed as early as 2 days after start of treatment, being most pronounced after 1 week. Hypothetical circulating blocking factors for cellular immune reactions might be present in the untreated syphilitic patient, which become abolished after therapy. Since stimulation with Con A of syphilitic leukocytes gave normal results even before treatment in the syphilitic patient, there might be a specific block of leukocyte migration inhibition against T.p.

Treponema pallidum protein Tp47 induced prostaglandin E2 to inhibit the phagocytosis in human macrophages

“…The host's immune system actively participates in the relentless pursuit and elimination of T. pallidum, while T. pallidum skillfully employs various mechanisms to evade immune recognition, such as suppression of host cellular immune responses. 34,35 Macrophages are the frontline cells of innate defence and play a crucial role in the process of T. pallidum infection. A previous study has demonstrated that Tp92, the outer membrane protein of T. pallidum, induces the death of human monocytes in the early stages of T. pallidum infection, which helps T. pallidum to escape recognition and elimination by the host innate immune system.…”

“…During T. pallidum infection, the interplay between the evasion strategies of T. pallidum and the host's innate and adaptive immune responses is a complex and dynamic battle. The host's immune system actively participates in the relentless pursuit and elimination of T. pallidum , while T. pallidum skillfully employs various mechanisms to evade immune recognition, such as suppression of host cellular immune responses 34,35 . Macrophages are the frontline cells of innate defence and play a crucial role in the process of T. pallidum infection.…”