A. M. Denman

The lymphocyte transformation test and gold hypersensitivity.

TheEmpireRheumatism Councils controlled trial (1960) showedthatgoldsalts benefit patients withrheumatoid arthritis. However, side-effects still occurwiththis treatment despite regular blood counts andurineexaminations and,although the incidence ofsevere reactions hasprobably been reduced bycareful attention tothedoseandnumber ofinjections given, serious haematological complications arestill encountered (Saphir andNey,1966). Itiswidely believed thattoxicity fromgoldtherapy isimmunologically determined, butsofarthere has beenlittle convincing evidence toprovethisassumption. Blast transformation ofperipheral bloodlymphocytes after their exposure invitro toanantigen towhichthedonorhasbecomesensitized hasbeen usedasa testfordrughypersensitivity (Vischer, 1966; Sarkany, 1967). We report hereexperiments inwhichtheperipheral bloodlymphocytes of patients withseveregoldtoxicity responded to invitrochallenge withMyocrisin. Theresults provide direct evidence thatgoldhypersensitivity isimmunologically determined andsuggest apossible methodforpredicting thelikelihood oftoxicity occurring inindividual patients.

CHANGES IN THE LIFE-SPAN OF CIRCULATING SMALL LYMPHOCYTES IN MICE AFTER TREATMENT WITH ANTI-LYMPHOCYTE GLOBULIN

Abstract The blood and lymphoid tissues of mice which had been injected with anti-lymphocyte globulin (A.L.G.) proved to be depleted particularly of long-lived small lymphocytes. The blood later became repopulated predominantly by shortlived small lymphocytes. This change in the composition of the circulating small-lymphocyte population, which was observed in intact animals and in mice thymectomised as adults, was not reflected in the absolute blood lymphocytecount. These findings indicate one mechanism by which A.L.G. exerts its prolonged immunosuppressive effects.

Immunosuppressive effects of lymphoid cell proliferation in mice receiving anti-lymphocyte globulin.

ANTILYMPHOCYTE serum (ALS) and globulin (ALG) are potent suppressors of certain forms of immune response, particularly homograft rejection1,2 and the primary antibody response3. Their mode of action has, however, been disputed. Although lymphopenia has been considered the essential cause of the immunosuppression4 it has not always accompanied homograft acceptance which is induced by these agents2,5. “Blind-folding” and “sterile blast activation” of lymphocytes by ALG have been proposed as alternative mechanisms2. It has also been observed that renal homografts which have escaped rejection can nevertheless be infiltrated by lymphocytes, suggesting that the progeny of lymphoid cells exposed to ALG function inadequately6.

SUPPRESSION OF COOMBS-POSITIVE HÆMOLYTIC ANAEMIA IN NZB MICE BY ANTILYMPHOCYTE GLOBULIN

Abstract The naturally occurring Coombs-positive haemolytic anaemia of NZB mice is suppressed by prior treatment with antilymphocyte globulin (A.L.G.) given from two months of age. This agent does not significantly affect the established disease in older mice. The transfer of positive antiglobulin (Coombs) reactions from old, affected to young, unaffected NZB mice by spleen cells was prevented by preincubation of these cells with A.L.G. The failure of A.L.G. to suppress the established disease can be explained in terms of its site of action.