12 research outputs found
Wound-healing activity of ethanolic and aqueous extracts of Ficus benghalensis
Wound healing is the process of repair that follows injury to the skin and other soft tissues. Following injury, an inflammatory response occurs and the cells below the dermis (the deepest skin layer) begin to increase collagen (connective tissue) production. Later, the epithelial tissue (the outer skin) is regenerated. There are three stages to the process of wound healing: inflammation, proliferation, and remodeling. Traditionally, Ficus benghalensis is used for wound healing. Since no detailed scientific data are available regarding the wound-healing activity of F. benghalensis, the present study was designed to explore the same. The wound-healing efficacy of ethanolic and aqueous extracts of F. benghalensis was evaluated in excision and incision wound models. The parameters studied include rate of wound contraction, period of complete epithelialization, and tensile strength of incision wound. Student′s t test was used to analyze the results obtained from the present study and P<0.05 was considered significant. Both the ethanolic and aqueous extracts of F. benghalensis were found to possess significant wound-healing activity, which was evidenced by decrease in the period of epithelialization, increase in the rate of wound contraction and skin-breaking strength. The present study has demonstrated that the ethanolic and aqueous extracts of F. benghalensis have properties that render them capable of promoting accelerated wound-healing activity compared with placebo control
Antigen-specific immunity does not mediate acute regression of UVB-induced p53-mutant clones
Antigen-specific immunity does not mediate acute regression of UVB-induced p53-mutant clones
An Hour after Immunization Peritoneal B-1 Cells Are Activated to Migrate to Lymphoid Organs Where within 1 Day They Produce IgM Antibodies That Initiate Elicitation of Contact Sensitivity
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B cell-dependent T cell responses: IgM antibodies are required to elicit contact sensitivity.
Contact sensitivity (CS) is a classic example of in vivo T cell immunity in which skin sensitization with reactive hapten leads to immunized T cells, which are then recruited locally to mediate antigen-specific inflammation after subsequent skin challenge. We have previously shown that T cell recruitment in CS is triggered by local activation of complement, which generates C5a that triggers C5a receptors most likely on mast cells. Here, we show that B-1 cell-derived antihapten IgM antibodies generated within 1 day (d) of immunization combine with local challenge antigen to activate complement to recruit the T cells. These findings overturn three widely accepted immune response paradigms by showing that (a) specific IgM antibodies are required to initiate CS, which is a classical model of T cell immunity thought exclusively due to T cells, (b) CS priming induces production of specific IgM antibodies within 1 d, although primary antibody responses typically begin by day 4, and (c) B-1 cells produce the 1-d IgM response to CS priming, although these cells generally are thought to be nonresponsive to antigenic stimulation. Coupled with previous evidence, our findings indicate that the elicitation of CS is initiated by rapidly formed IgM antibodies. The IgM and challenge antigen likely form local complexes that activate complement, generating C5a, leading to local vascular activation to recruit the antigen-primed effector T cells that mediate the CS response