Due to the increasing prevalence and number of life-threatening cases, food allergy has emerged as a major health concern. The classic immune response seen during food allergy is allergen-specific IgE sensitization and hypersensitivity reactions to foods occur in the effector phase with often severe and deleterious outcomes. Recent research has advanced understanding of the immunological mechanisms occurring during the effector phase of allergic reactions to ingested food. Therefore, this review will not only cover the mucosal immune system of the gastrointestinal tract and the immunological mechanisms underlying IgE-mediated food allergy, but will also introduce cells recently identified to have a role in the hypersensitivity reaction to food allergens. These include IL-9 producing mucosal mast cells (MMC9s) and type 2 innate lymphoid cells (ILC2s). The involvement of these cell types in potentiating the type 2 immune response and developing the anaphylactic response to food allergens will be discussed. In addition, it has become apparent that there is a collaboration between these cells that contributes to an individual's susceptibility to IgE-mediated food allergy.
Allergens ; Cooperative Behavior ; Food Hypersensitivity* ; Gastrointestinal Tract ; Hypersensitivity ; Immune System ; Immunoglobulin E ; Interleukin-9* ; Lymphocytes* ; Mast Cells* ; Prevalence

Recently we experienced a soft tissue sarcoma originated in the spinal epidural space at upper sacral area and extending into intrapelvic area in a young male patient. It was diagnosed primary Ewing's sarcoma histologically. Ewing's sarcoma is usually found in long bones. But rarely discovered in an extraosseous area. So, spinal epidural Ewing's sarcoma is rare to be found. Only 6 cases were reported in the English literature until 1986. We present the case with review of literatures.
Epidural Space ; Humans ; Male ; Sarcoma ; Sarcoma, Ewing*

BACKGROUND: In addition to TCR and costimulatory signals, cytokine signals are required for the differentiation of activated CD8 T cells into memory T cells and their survival. Previously, we have shown that IL-12 priming during initial antigenic stimulation significantly enhanced the survival of activated CD8 T cells and increased the memory cell population. In the present study, we analyzed the mechanisms by which IL-12 priming contributes to activation and survival of CD8 T cells. METHODS: We observed dramatically decreased expression of CD43 in activated CD8 T cells by IL-12 priming. We purified CD43(lo) and CD43(hi) cells after IL-12 priming and analyzed the function and survival of each population both in vivo and in vitro. RESULTS: Compared to CD43(hi) effector cells, CD43(lo) effector CD8 T cells exhibited reduced cytolytic activity and lower granzyme B expression but showed increased survival. CD43(lo) effector CD8 T cells also showed increased in vivo expansion after adoptive transfer and antigen challenge. The enhanced survival of CD43(lo) CD8 T cells was also partly associated with CD62L expression. CONCLUSION: We suggest that CD43 expression regulated by IL-12 priming plays an important role in differentiation and survival of CD8 T cells.
Adoptive Transfer ; Granzymes ; Interleukin-12 ; Memory ; T-Lymphocytes

The authors analyzed 72 cerebral stroke with diabetes mellitus who were admitted to our hospital during 1989 to 1993. Pathophysiology and clinical characteristic complication and mortality was analyzed. Followings are results: 1) Among 398 total cerebral stroke who were hospitalized to our hospital during 1989 to 1993, there were 72 cerebral stroke with diabetes(18%). 2) The rate of cerebral infarction and hemorrhage was 67% and 33%. The infarction rate was much higher compared with it of general cerebral stroke. 3) Various complications were presented and mortality rate was 24.% which was regarded higher than it of general cerebral stroke. 4) Association of mortality, prognostic index and other variables were analyzed.
Cerebral Hemorrhage ; Cerebral Infarction ; Diabetes Mellitus* ; Hemorrhage ; Humans ; Infarction ; Mortality ; Stroke*