To demonstrate human leukocyte antigen (HLA)-linked control of susceptibility to pulmonary tuberculosis, 25 multiple-case families were tissue typed for class I and class II HLA specificities. Eight non-HLA genetic markers were also examined for any indication of other genetic factors that might influence the Mycobacterium tuberculosis infection. Observations on estimated HLA haplotype segregation in the sibs suggest that 84% of the affected sibs shared significantly more often than expected a common haplotype with each other than the normal unaffected sibs (P less than 0.001). Also, there was a skewed transmission of DR2 to diseased offspring from diseased parents (21 of 27) and to diseased offspring from healthy parents (15 of 17) in contrast to the transmission of DR2 from either group of parents to healthy offspring (six of 15 and 10 of 16, respectively). The segregation of non-HLA polymorphisms did not deviate significantly from the expected figures. These data provide strong evidence in favor of DR2-associated susceptibility to pulmonary tuberculosis.

Investigations for the HLA-A, -B, -C and -DR antigens were conducted on 124 random North Indian patients with confirmed diagnosis of pulmonary tuberculosis by the demonstration of acid fast bacilli in the sputum. 109 appropriately matched controls from the same ethnic background were also tissue typed. No significant deviation was observed in the HLA-A, -B, and -C locus antigens. With the HLA-DR typing, there was a marginal increase in DR2 and a concurrent significant decrease in DRw6 in the patient group. These deviations were, however, insignificant when correction for the P value was made. ABO blood group typing results indicate that blood group '0' may afford protection against TB. The involvement of both DR2 and DRw6 is interesting as it is also implicated in leprosy, another mycobacterial disease. The results suggest the possibility of a common gene in the MHC for both tuberculosis and leprosy.

Twenty‐five multiple case families of pulmonary tuberculosis were HLA typed and the data analysed by the lod score method. There was no evidence of linkage between the susceptibility gene and pulmonary TB, though there were consistently positive female scores. A number of other chromosome 6 genetic markers tested did not reveal any significant deviation in the patient group as cornpared to the controls, except GLO 2‐ 1 which occurred with a significantly decreased frequency in the former.