Soluble HLA class I molecules in malignant pleural and peritoneal effusions and its possible role on NK and LAK cytotoxicity
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Published on: July 21, 2016
Z Amirghofran1, A K Sheikhi, P V Kumar
1Department of Immunology, Shiraz University of Medical Sciences, Shiraz 71345-1798, Iran. amirghz@sums.ac.ir
Insights
Soluble HLA class I (sHLA-I) molecules are present in malignant effusions, suggesting a role in tumor immunity. However, sHLA-I levels did not significantly correlate with effusion-associated lymphoid cells' killing activity.
Area of Science:
- Immunology
- Oncology
Background:
- Soluble HLA class I (sHLA-I) molecules are implicated in immune responses.
- Their role in malignant effusions and natural immune defense requires further investigation.
Purpose of the Study:
- To quantify sHLA-I levels in malignant pleural and peritoneal effusions.
- To explore the potential role of sHLA-I in natural immune defense mechanisms within these effusions.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) was used to measure sHLA-I levels in effusions from patients with malignancy, infection, or other diseases.
- Cytolytic activity of effusion-associated lymphoid (EAL) cells was assessed via co-culture with autologous cell-free effusions and IL-2 stimulation.
Main Results:
- Mean sHLA-I levels were higher in malignant and infected effusions compared to other diseases, but differences were not statistically significant.
- EAL cells from malignant and infected effusions showed comparable killing activity, which was not correlated with sHLA-I levels.
- Exposure to malignant effusions increased NK cell activity and decreased LAK cell activity in EAL cells, independent of sHLA-I concentration.
Conclusions:
- The presence of sHLA-I in malignant effusions suggests a potential role in tumor immunity.
- sHLA-I does not appear to be the sole determinant of EAL cell killing activity in these effusions.
- Further research is needed to fully elucidate the function of sHLA-I in the tumor microenvironment.
Purpose:
To examine the amount of sHLA-I in malignant pleural and peritoneal effusions and its possible role in natural immune defense.
Methods:
Three groups of patients (75 patients with malignancy, 21 with infection, and 27 with other diseases) were studied for sHLA-I value using an ELISA method. Cytolytic activity of freshly isolated pleural and peritoneal effusion-associated lymphoid (EAL) cells from 14 of cases with malignancy were examined and compared to that of ten non-cancerous patients. EAL cells were co-cultured with the autologous cell-free effusions immediately after collection and 3 days after incubation with IL-2.
Results:
The mean value of sHLA-I in effusions was 1.01+/-1.36 micro g/ml, 0.97+/-1.20 micro g/ml, and 0.49+/-0.45 micro g/ml, respectively. Despite higher mean sHLA-I levels in malignant and infected patients, no significant difference between these groups was observed ( P >0.05). Generally, the amount of sHLA-I in peritoneal effusions was higher than that for pleural effusions, but the difference was not significant. There were also no statistical differences in the sHLA-I levels between sub-groups of patients with malignancy. EAL cells' killing activity in malignant and infected effusions was 68.15+/-11.73 and 78.28+/-14.41, respectively ( P=0.08). No correlation between sHLA-I level and NK activity of EAL cells from the patients was found. Almost all malignant cases after exposure to cell-free effusions displayed an increase in NK activity (from 68.66+/-11.13 to 74.2+/-12.39, P=0.042) and a decrease in LAK activity (74.5+/-18.30 vs 67.72+/-16.46, P=0.040). Whereas, the same experiment performed for non-malignant effusions showed a decrease in both NK activity and LAK activity. Changes in NK and LAK activity were not correlated with the amount of sHLA-I in the effusions.
Conclusion:
The presence of sHLA-I, particularly in malignant effusions, suggests a role for these molecules in tumor immunity in the peritoneal or plural environment; however, at least with these group of patients, sHLA-I appears not to be a unique determining factor on EAL cells' killing activity.
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