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Biomedical subjects

V Haridas

Publications and source records attributed to V Haridas.

26 records · Page 2Linked to original sources
PubMed1995

Role of major histocompatibility complex class I antigens in modulating the performance of murine tumour cells in cold target competition assays.

The role of class I major histocompatibility complex (MHC) antigen levels on the ability of five murine tumour cell lines (YAC, P815, EL4, SP20 and L929) to competitively inhibit their own lysis, as well as the lysis of other targets by lymphokine-activated killer (LAK) effector cells was examined. Basal LAK susceptibilities of the cell lines were in the order P815 > YAC > SP20 > EL4 > L929, whereas the basal class I MHC antigen levels were in the order P815 > SP20 > L929 > YAC > EL4. Treatment with interferon-gamma (IFN-gamma) induced augmentation of class I MHC antigen levels on all cell lines. A concomitant decline in LAK susceptibility was seen for P815, YAC, SP20 and L929 cells, but not for EL4 target cells. On the basis of competition results, tumour cells appear to fall into two groups (group 1: P815, YAC and SP20; group 2: EL4 and L929). Members of each group could in general competitively inhibit the lysis of cell lines of their own group only. Treatment with IFN-gamma suppressed the ability of all tumour cell lines, except EL4, to cause competitive inhibition. These results support the proposition that class I MHC antigens may interfere with the recognition of target cells by effector LAK cells.

Animals↗
PubMed1994

Effect of gamma interferon on the expression of class I MHC antigens on fresh leukemic cells and their susceptibility to lysis by lymphokine activated killer cells.

Relationship between MHC class I antigen expression on PBLs from leukemia patients and their susceptibility to lysis by LAK cells was investigated. LAK cells induced small yet significant lysis of leukemic cells. In nine out of 14 cases studied, treatment with Interferon gamma (200 U/ml for 48 hours) resulted in a decrease in the LAK susceptibility of leukemic cells. In six of these cases, there was a concomitant increase in the expression of class I MHC antigen expression. In three samples, the increase in MHC class I antigen expression was not accompanied by a decrease in LAK susceptibility. IFN treatment had no effect on the binding of leukemic cells to LAK effector cells.

Down-Regulation↗
PubMed1993

MHC class I up-regulation protects some but not all targets against LAK-mediated lysis: possible implications for the existence of LAK cell subpopulations using different recognition strategies.

The effect of gamma-interferon (gamma-IFN) was examined on the lymphokine-activated killer (LAK) cell susceptibility and the levels of major histocompatibility complex (MHC) class I antigen expression on YAC, P815 and EL4 cells. IFN induced a marked increase in the MHC class I antigen expression on all target cells, a concomitant decrease in LAK sensitivity was observed for YAC and P815 cells but not for EL4 cells. In competition experiments, lysis of YAC cells by LAK cells was inhibited by control or IFN-treated YAC and P815 cells, but not by control or IFN-treated EL4 cells. Moreover, lysis of EL4 cells was not inhibited by control or IFN-treated YAC cells. Our results suggest that the effectors killing EL4 are distinct from those killing YAC and/or P815 and that the former are not influenced by the levels of MHC class I antigens on target cells.

Animals↗
PubMed1993

Evaluation of particle agglutination test for detection of HIV-I antibodies.

A commercially available particle agglutination test (PA) was evaluated for its specificity and sensitivity as compared to ELISA currently used in our laboratory to detect HIV-I antibodies. A total of 463 sera from blood donors and clinical referrals were screened by PA, 45 were found to be positive (9.7%). Out of 463, 258 sera were simultaneously screened by ELISA; 28 were found to be positive (10.8%). Twelve samples showing positive results by both ELISA & PA were tested by Western blot and were confirmed to be positive. We found sensitivity of PA as compared to ELISA as 100% and specificity to be 88.44%. Readings of PA taken at 2 hrs should be reconfirmed at 24 hrs as it eliminates a number of false positives. Overall, we feel PA is fairly comparable with ELISA. It can be used in the set up where equipment and trained personnel for ELISA are not available for primary screening purposes.

Agglutination Tests↗
PubMed1990

Immune response to hepatitis B viral antigens in chronic infection & its relationship with liver necrosis.

Markers of hepatitis B virus (HBV) and immune response against them were studied in 18 chronic asymptomatic carriers, 8 patients of the virus induced chronic liver disease (CLD), and 7 patients of chronic alcoholic liver cirrhosis, who were also chronic HBV carriers (CALC). The LMI responses to HBeAg were elevated in HBeAg and/or HBV-DNA positive chronic asymptomatic carriers, (median response 31.5%), along with elevation of serum alanine aminotransferase (sALT) levels (59-150 IU/l). On the other hand the LMI responses to this antigen, in HBeAg and HBV-DNA negative chronic carriers were in the normal range (median response 12%) and their sALT levels were also normal (7-50 IU/l). The CLD and CALC patients did not show any relation between their LMI to HBeAg and sALT levels. In contrast no relation between LMI to HBsAg and sALT levels was observed in any group. The LMI responses to HBsAg in CLD patients were elevated (median response 38%) and the responses of chronic asymptomatic carriers and CALC patients were either in the normal range or poor (median responses, 18 and 7% respectively), irrespective of their sALT levels. These results suggest that T cell responses to both the antigens may be involved in liver cell damage.

Chronic Disease↗
PubMed1988

Anti-idiotypic humoral and cellular responses to antibody to hepatitis B surface antigen in hepatitis B viral infections.

In order to investigate regulatory significance of humoral and cellular responses to the idiotypic (Id) determinants on the antibody to hepatitis B surface antigen (anti-HBs), they were studied in acute hepatitis B and in chronic HBV infection. The results were compared with humoral and cellular responses of the same patients to hepatitis B surface antigen (HBsAg). In acute hepatitis B, the responses to HBsAg, were delayed until 3-4 weeks after the onset of clinical symptoms. However, the leucocyte migration inhibition (LMI) and the lymphocyte transformation (LTT) responses to affinity purified anti-HBs were found to be evolved very early in the course of acute hepatitis B, though anti-Id antibodies were absent. The majority of chronic HBV carriers showed a poor humoral and cellular response to HBsAg. Ten out of 38 chronic carriers showed anti-Id antibodies which recognized a major cross-reactive idiotype (CRI) on the anti-HBs molecule. Twenty-five out of 38 chronic carriers also showed LMI response to the Id determinants on the anti-HBs. LMI response induced by anti-HBs could be blocked by a specific Balb/c anti-Id antibody which also recognized the CRI. Thus, in both acute and chronic HBV infections, the anti-Id humoral and cellular responses correlated with poor humoral and cellular responses to HBsAg, indicating regulatory significance.

Acute Disease↗