Regarding numerical changes of leukocytes involved in immune defects following thermal injury, a lot of controversial results have been reported. In this study, the changes of leukocyte number and distribution were examined and compared in spleen and lymph nodes of thermally injured mice. Mice (Balb/c) were anesthetized by intraqeritoneal injection of 2,2,2-tribromoethanol and thermally injured by immersion of hair-removed dorsal skin (15% total body surface) in a boiling water bath (96`C) for 7 seconds. Both of lymph node cell (LNC) and spleen cell (SPC) numbers decreased significantly at day 2 of injury and thereafter rebounded, but in a distinct pattern; 1) LNC numer returned to over normal level at day 6 and normalized again, whereas SPC number increased gradually over normal level and sustained until day 24 of injury. 2) Such increase of LNC and SPC number coincided with higher proportion of PMN and relative decline of lymphacytes, particularly CD3 T cells rather than slg' B cells, but such alteration was more significant in spleen. The changes of peripheral blood leukocyte (PBL) number was comparable to those of SPC. These data suggest that the cause of immune modulation in thermally injured mice acts systemically. In addition, it is noteworthy that reduction of lymphocyte and CD3 T cell proportions was due to relative increase of PMN number, not the decrease of absolute number of lymphocytes. Spontaneous recovery of injured mice in this study also implicates that increase of PMN number may be responsible for recovery from injury without infection. Finally, the CD4'/CD8' ratio of injured mice was lower only at day 2 ot injury, but not significantly, than that of control group. It is likely that contribution of Th/Ts ratio to immune defect after thermal injury should be determined together with other factors, such as injured body surface % and severity of injury.
Mice ; Animals

An activation antigen, CD30 was initially identified on Hodgkin and Reed-Sternberg (H-RS) cells. CD30 expression is observed on activated, but not on resting, T and B lymphocytes. Despite of numerous studies, the functions of CD30 in physiological condition remains open question. Moreover, CD30 expression of normal B lymphocytes has been poorly documented. In this study, CD30 expression of murine B lymphocytes and its regulation was analyzed. Murine splenic B (SP-B) cells obtained by adherence were used for activation with LPS or plate-bound anti-mouse IgM. LPS stimulation resulted in B cell proliferation. However, stimulation with plate-bound anti- mouse IgM (pb anti-mlgM) induced blast cell formation but did not increase cell number. Both stimulation induced minimal expression of CD30. Substantial CD30 expression of SP-B cells was induced by IL 4, which upregulated both of proliferation and CD30 expression of activated SP-B cells. Highest level of CD30 expression was detected at day 3 of stimulation. IL 2 enhanced B cell proliferation but not CD30 expression and rather reduced IL 4-mediated upregulation of CD30 expression. These data suggest that the signaling pathway for B cell proliferation is different from that for induction of CD30 expression and IL 4 exerts a pivotal role in CD30 expression of both T and B cells. In addition, T and B cells may show distinct response to other cytokines such as IL 2 in CD30 expression.
Animals ; Antigens, CD30 ; B-Lymphocytes* ; Cell Count ; Cell Proliferation ; Cytokines ; Immunoglobulin M ; Mice ; Up-Regulation

No abstract available.
Animals ; Asthma* ; Mice*

No abstract available.
Animals ; B-Lymphocytes* ; Mice*

No abstract available.

No abstract available.

In the present study, we have tried to isolate and identify herpes simplex virus type 2(HSV 2) from clinical specirnens, which were inoculated into Vero cell line and grown. Eight strains of viruses were isolated from 20 suspected cases diagnosed from the pr ivate clinics in Seoul. Viruses isolated from 4 rnale and 1 female cases with active lesion were identified to the HSV 2 by indirect immunofluorescence using monoclonal antibody to HSV-2. In addition, morphology of the isolated viruses were observed under electron microscope.
Female ; Fluorescent Antibody Technique, Indirect ; Herpes Simplex* ; Herpesvirus 2, Human* ; Humans ; Seoul ; Simplexvirus* ; Vero Cells

To evaluate characteristic CT findings of orbital pseudotumor and to define differentialpoints from other pathology, the authors retrospectively reviewed CT of 19 patients who were prooen to have orbital pseudotumor by clinical course and, in some cases, biopsy. A variety of CT findings including extraocular muscle thickening(11 cases), streaky infiltration of retroorbital fat(11 cases), mass formation(10 cases), optic nerve thickening (6 cases), conjunctival thickening (5 cases), scleral thickening(4cases), enlarged lacrimal gland(4 cases) and destruction of orbital bone (2 cases) were observed. Thickening of the anterior portion and irregular margin were characteristic findings of extraocular muscle and optic nerve lesions. Mass formation predominantly occurs in the anterior portion of the orbit. In most cases more than two orbital structures are involved by lesion.
Biopsy ; Humans ; Optic Nerve ; Orbit* ; Orbital Pseudotumor* ; Pathology ; Retrospective Studies

BACKGROUND: CD30 is a member of TNF receptor family and expressed on lymphocytes and other hematopoietic cells following activation as well as Hodgkin and Reed- Sternberg cells in Hodgkin's lymphoma. In this study, CD30-mediated regulation of cell adhesion molecule expression on normal activated mouse T cells was investigated. METHODS: Mouse T cells were activated with anti-CD3 antibody for induction of CD30, which was cross-linked by immobilized anti-CD30 antibody. RESULTS: High level of CD30 expression on T cells was observed on day 5, but only little on day 3 even under culture condition resulting in an identical T cell proliferation, indicating that CD30 expression requires a prolonged stimulation up to 5 days. Cross-linking of CD30 alone altered neither proliferation nor apoptosis of normal activated T cells. Instead, CD30 appeared to promote cell adherence to culture substrate, and considerably upregulated ICAM-1 and, to a lesser extent, ICAM-2 expression on activated T cells, whereas CD2 and CD18 (LFA-1) expression was not affected. None of cytokines known as main regulators of ICAM-1 expression on tissue cells (IL 4, IFNgamma and TNFalpha) enhanced ICAM-1 expression in the absence of CD30 signals. On the other hand, addition of NF-kappaB inhibitor, PDTC (0.1 mM) completely abrogated the CD30-mediated upregulation of ICAM-1 expression, but not CD2 and ICAM-2 expression. CONCLUSION: This results support that CD30 upregulates ICAM-1 expression of T cell and such regulation is not mediated by higher cytokine production but NF-kappaB activation. Therefore, CD30 may play important roles in T-T or T-B cell interaction through regulation of ICAM-1, and -2 expression.
Animals ; Apoptosis ; Cell Adhesion Molecules ; Cell Adhesion* ; Cell Communication ; Cell Proliferation ; Cytokines ; Hand ; Hodgkin Disease ; Humans ; Intercellular Adhesion Molecule-1 ; Lymphocytes ; Mice ; NF-kappa B ; Receptors, Tumor Necrosis Factor ; T-Lymphocytes* ; Up-Regulation

Cellular oncogenes are expressed as an intrinsic part of the transformed or neoplastic phenotype. More than 60 of the known cellular oncogenes play a specific role in normal cellular development and differentiation. To examine the correlation between ras oncogene expression and the development of cervical cancer, this study investigated the reactivity of cervical intraepithelial neoplasia(CIN) and carcinoma of the uterine cervix by using anti-ras P21 mouse monoclonal antibody. The expression of ras oncogene significantly increased with the grade of malignancy from 11% in severe dysplasia, 30% in carcinoma in situ, 43% in microinvasive carcinoma, to 53% in invasive cancer. The expression of ras oncogene was not correlated with histologic type, tumor size, and nodal status of cervical cancer. It was concluded that expression of ras oncogene is related to early phase of carcinogenesis and tumor invasion of carcinoma of the uterine cervix.
Animals ; Carcinogenesis ; Carcinoma in Situ ; Cervix Uteri* ; Female ; Genes, ras* ; Mice ; Oncogenes ; Phenotype ; Uterine Cervical Neoplasms