L. Mutti et al., PRIMARY HUMAN MESOTHELIOMA CELLS EXPRESS CLASS-II MHC, ICAM-1 AND B7-2 AND CAN PRESENT RECALL ANTIGENS TO AUTOLOGOUS BLOOD-LYMPHOCYTES, International journal of cancer, 78(6), 1998, pp. 740-749
Mesothelioma cells (MMc) are considered to be weakly immunogenic and t
he experimental approaches attempting to induce an immune response aga
inst these cells have been disappointing, Our aim was to investigate w
hether MMc possess the surface accessory molecules involved in antigen
presentation and whether these cells are capable of presenting recall
antigens to autologous blood lymphocytes. pour primary MMc cultures w
ere generated from malignant effusions and examined to assess whether
the accessory molecules required for antigen presentation were present
on their surfaces, Intercellular adhesion molecule-1 (ICAM-1; CD54):
class I and class II major histocompatibility complex-DR (MHCI and MHC
II-DR); B7-1 (CD80.3); and B7-2 (CD86) expression by MMc was studied b
y immunocytochemical and/or FACScan analysis. MMc were pulsed with pur
ified protein derivative (PPD), Tetanus toroid (TT) and Candida albica
ns (CA) bodies, and incubated with autologous lymphocytes, Lymphocyte
proliferation was estimated by radionucleotide incorporation, Phenotyp
ic analysis showed the presence of MHCII-DR, ICAM-1 and 87-2 on primar
y MMc cultures, whereas the phenotypic evaluation of 2 established MMc
lines did not show the presence of the B7-1 and B7-2 molecules. In ad
dition, MHCII-DR was detectable only after interferon gamma (IFN-gamma
) stimulation. Primary MMc cultures acquired the capability to induce
lymphocyte proliferation after pulse with the recall antigens, To achi
eve characterization of these lymphocytes, we generated a PPD-specific
CD4(+) T-cell clone. PPD-pulsed MMc were shown to specifically induce
T-cell clone proliferation through a MHCII-DR-mediated process. We co
nclude that primary MMc possess the surface molecules required for ant
igen presentation and can present recall antigens to CD4(+) lymphocyte
s, (C) 1998 Wiley-Liss, Inc.