Keiichiro Matsunaga

Segmental portal hypertension in mixed connective tissue disease

A 64-year-old Japanese woman was diagnosed with mixed connective tissue disease based on the clinical evidence; myositis with infiltration of CD45RO+ T cells and histiocytes, interstitial pneumonia, isolated high titer of anti-U1RNP antibody and hypocomplementemia. Endoscopic examination revealed gastric varices due to isolated splenic vein obstruction. Antiphospholipid antibody, antilymphocyte antibody, anti-U1RNP antibody and miscellaneous pathogens from the intestines were possible causes for obstruction of the splenic vein.

EPIDERMAL CELLS BEARING BOTH I‐A AND I‐E SUBREGION ANTIGENS CAN INDUCE HEN EGG WHITE LYSOZYME‐SPECIFIC T LYMPHOCYTE PROLIFERATION*

Antigen‐primed T lymphocytes require accessory cells to initiate a proliferative response. These cells have been designated antigen presenting cells. In the present investigation, we found that immune associated antigen (Ia) bearing, mouse epidermal cells possess antigen presenting activity. These epidermal cells also display substantial levels of mixed lymphocyte reaction (MLR) activity. However, this MLR of itself did not suppress nor enhance antigen presenting activity. Genetic mapping studies demonstrated that compatibility at the I‐A and I‐E subregions of the MHC is important for effective presentation of either lysozyme or ovalbumin. In vitro inhibition and blocking studies using alloantisera confirmed that I‐A and I‐E gene products of these epidermal cells may play an important role in the interaction of primed T lymphocytes and antigen‐pulsed epidermal cells. In addition, epidermal cells bearing Fc and C3 receptors on the cell surfaces were more efficient at inducing the lymphocyte proliferation than were epidermal cells depleted of these cells. These results suggest that Ia positive epidermal cells may be involved in the initiation of delayed type hypersensitivity reactions through antigen recognition followed by antigen presentation and T lymphocyte proliferation.