In rheumatic fever the antibodies previously formed against steptococcal cell wall antigen will later cross react with a look-alike self Ag present on the myocardial cell. When they react they cause a local tissue damage. In type II, the Ab-Ag reaction occurs and damages locally.
In Post Streptococcal Glomerulonephritis the same Ab-Ag complexes are wandering in the circulation and then get deposited in the glomeruli. In Type III, preformed immune complexes cause remote (not local) damage.
In rheumatic fever, the antibodies generated against streptococcal antigens cross react with many target tissues in the body resulting in molecular mimicry. So damages result from cellular interaction between antigen and antibody and it is regarded as type II H/S(cytotoxic).
In PSGN, the circulating immune complexes in the serum resulting from streptococcal infection become deposited in the kidney. Damages are due to the immune complexes and it is regarded as type III H/S(immune complex).