Kiyoshi Katoh

Pathologic features of Behçet's syndrome: A review of Japanese autopsy registry data

The data recorded from 170 autopsies of patients with Behçets syndrome in Japan during the period from 1961 to 1976 were analyzed. The patients had been in the second to the eighth decade of life, and the ratio of males to females was 5 to 2. A wide spectrum of pathologic findings was observed, with involvement of neurologic, ophthalmic, cardiovascular, pulmonary, gastrointestinal, visceral, genitourinary, and mucocutaneous systems. Some of the common acknowledged clinical features of the syndrome, such as oral ulcers, synovitis, retinal and cutaneous vasculitis, and venous occlusions, were underreported. This apparent discrepancy in an autopsy series may be due to the effects of treatment or the healing process, as well as to the possible incompleteness of the postmortem examination. The accessibility of recorded data in a national autopsy registry offers a unique opportunity for review of the pathologic features of Behçets syndrome.

Differentiation between schwannoma of the vagus nerve and schwannoma of the cervical sympathetic chain by imaging diagnosis.

Ultrasonography, computed tomography, and magnetic resonance imaging were performed to differentiate preoperatively between schwannomas of the vagus nerve and schwannomas of the cervical sympathetic chain by observing the position of schwannomas in regard to the surrounding blood vessels. Ultrasonography also permitted direct visualization of the vagus nerve, so its position relative to the schwannoma could be examined.

Establishment of monoclonal antibodies which possess the same characteristics as the naturally occurring thymocytotoxic autoantibodies (NTA)

SummaryAutoantibody-secreting hybrid cell lines were obtained by fusion of spleen cells from unimmunized (NZB×NZW) F1 mice with the HAT-sensitive mouse myeloma cell line SP2/0-Ag14. Eight hybridoma cell lines producing autoantibodies to mouse thymocytes were cloned and the resultant antibodies were partially characterized. All eight monoclonal antibodies lysed mouse thymocytes in the presence of rabbit complement. The anti-thymocyte cytotoxic antibody activities were absorbed with thymocytes, lymph node cells, unfractionated spleen cells, and splenic T cells; but not with bone marrow cells, splenic B cells, or homogenates of mouse kidney, liver, or striated muscle cells. In addition, the cytotoxic activities of culture supernatants from seven of the eight hybrid clones were absorbed with mouse brain tissue homogenates. Isotyping of the monoclonal antibodies revealed that five were IgM and three were IgG2a. Mouse thymocytes sensitized with each of the eight monoclonal antibodies in vitro became highly susceptible to phagocytosis by syngeneic macrophages. The monoclonal antithymocyte antibodies, thus, appear to be similar to the naturally occurring, (NZB×NZW) F1 thymocytotoxic autoantibodies (NTA) described by Shirai et al. [20–23].

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.