PMID- 10447737 OWN - NLM STAT- MEDLINE DCOM- 20000404 LR - 20190513 IS - 0019-2805 (Print) IS - 1365-2567 (Electronic) IS - 0019-2805 (Linking) VI - 97 IP - 2 DP - 1999 Jun TI - Administration of interleukin-12 exerts a therapeutic instead of a long-term preventive effect on mite Der p I allergen-induced animal model of airway inflammation. PG - 232-40 AB - Interleukin-12 (IL-12) is a key cytokine, which promotes T helper type 1 (Th1) cell-mediated immunity and inhibits Th2-type responses. It has been previously shown that IL-12 administration during active immunization following a single allergen exposure can prevent antigen-induced increases in immunoglobulin E (IgE) formation, Th2 cytokine production and bronchoalveolar lavage (BAL) eosinophils in a murine model of allergic airway inflammation. Thus, these studies have now been extended and two IL-12 treatment protocols on this murine model were evaluated. Administration of IL-12 during the active immunization strikingly increased Der p I-specific serum IgG2a and transiently decreased the levels of IgG1 and IgE antibodies following multiple allergen challenges. Such early treatment of IL-12 down-regulated IL-5 production and modestly up-regulated interferon-gamma production but did not effect BAL eosinophilia. These results suggest that repeated exposure to antigen and IL-12 is necessary to maintain a persistent Th1-recall response. Furthermore, administration of IL-12 to actively immunized mice, in which Th2-associated responses were established, had a significant effect on IgG2a synthesis and a modest effect on IgE levels, also down-regulation of IL-5 production, and markedly increased interferon-gamma production and abolished recruitment of eosinophils. Therefore, these data indicate that IL-12 can inhibit antigen-induced eosinophil infiltration into airways, despite the existence of a Th2-associated response. Taken together, these studies suggest that IL-12 may be useful as an immunotherapeutic agent in the treatment of such pulmonary allergic disorders as bronchial asthma. FAU - Lee, Y AU - Lee Y AD - Graduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei, Taiwan. FAU - Fu, C AU - Fu C FAU - Chiang, B AU - Chiang B LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - Immunology JT - Immunology JID - 0374672 RN - 0 (Allergens) RN - 0 (Antigens, Dermatophagoides) RN - 0 (Glycoproteins) RN - 0 (Immunoglobulin G) RN - 0 (Recombinant Proteins) RN - 187348-17-0 (Interleukin-12) RN - 37341-29-0 (Immunoglobulin E) SB - IM MH - Allergens/*immunology MH - Animals MH - Antigens, Dermatophagoides MH - Cell Division/immunology MH - Female MH - Glycoproteins/*immunology MH - Immunization MH - Immunoglobulin E/biosynthesis MH - Immunoglobulin G/biosynthesis MH - Interleukin-12/*therapeutic use MH - Mice MH - Mice, Inbred C57BL MH - Mites/*immunology MH - Recombinant Proteins/therapeutic use MH - Respiratory Hypersensitivity/immunology/*therapy MH - T-Lymphocytes/immunology PMC - PMC2326828 EDAT- 1999/08/14 10:00 MHDA- 2001/07/04 10:01 PMCR- 2000/06/01 CRDT- 1999/08/14 10:00 PHST- 1999/08/14 10:00 [pubmed] PHST- 2001/07/04 10:01 [medline] PHST- 1999/08/14 10:00 [entrez] PHST- 2000/06/01 00:00 [pmc-release] AID - imm768 [pii] AID - 10.1046/j.1365-2567.1999.00768.x [doi] PST - ppublish SO - Immunology. 1999 Jun;97(2):232-40. doi: 10.1046/j.1365-2567.1999.00768.x.