Humoral immunity, demonstrated by antibody production or antiserum injection, significantly increased the severity and prevalence of obstructive coronary lesions in transplanted mouse hearts (p<0.0003).
Does humoral immunity drive the development of obstructive coronary lesions in transplanted mouse hearts?
Humoral immunity plays a primary role in the development of atheromatous changes and obstructive coronary lesions in transplanted hearts.
p-value: p=< 0.0003
Obstructive lesions in arterial vessels of transplanted organs constitute an important factor in the late failure of these organs, especially for the heart. The absence of obstructive lesions in syngeneic donor-recipient combinations, suggests that they depend upon recipient immune responsiveness. It is controversial whether humoral or cellular aspects of the immune response predominate in the process. The present experiments employed hearts transplanted between inbred mice. After brief preoperative immunosuppression of recipients with mAbs to CD4 and CD8 determinants, hearts transplanted between mice incompatible for histocompatibility Ags survived for prolonged periods and most developed typical, obstructive coronary lesions. Our quantitative scoring of vascular changes on tissue sections of excised hearts, grades both their severity and prevalence. Transplants between strains that produced Abs to donor cells (B10.A to B10.BR), developed coronary lesions exceeding those in the reverse combination in which no detectable Ab was formed (B10.BR to B10.A; p < 0.00001), even though their histoincompatibility was similar. Treatment of B10.A recipients of B10.BR hearts with an antiserum against the donor significantly increased coronary lesions (p < 0.0003) in a dose-dependent fashion. Coronary arteries of B10.BR hearts transplanted to C.B-17 SCID mice remained largely free of lesions, whereas transplants to SCID recipients that received continuing injections of an antiserum directed to Ags of the donor developed striking, obstructive coronary lesions. We conclude that humoral immunity can be the prime instigator of atheromatous changes that occur in transplanted hearts.
Russell et al. (Sun,) conducted a other in Coronary atherosclerosis in transplanted hearts. Antiserum against donor antigens vs. No antiserum / strains not producing antibodies to donor cells was evaluated on Severity and prevalence of obstructive coronary lesions (p=< 0.0003). Humoral immunity, demonstrated by antibody production or antiserum injection, significantly increased the severity and prevalence of obstructive coronary lesions in transplanted mouse hearts (p<0.0003).