Yale School of Medicine

Internal Medicine

Internal Medicine, Yale School of Medicine

Internal Medicine
333 Cedar Street
Room LMP-1072
P.O. Box 208056
New Haven, CT 06520-8056

Philip W. Askenase, M.D.

Philip W. Askenase, M.D.

Professor of Medicine and Pathology Chief, Section of Clinical Immunology and Allergy

Research Interests

The focus of our work is the dissection of crucial cellular and molecular interactions guiding the traffic and eventual recruitment of antigen-specific T cells, out of the blood vessels, and into the tissues, at specific sites of immune reactivity, such as allergic responses (asthma) or protective responses, such expulsion of helminth worms from the GI tract, or ticks from the skin.

We have identified that micro-mediators, such as serotonin and leukotrienes, released by mediator-containing cells, such as mast cells or platelets, are of crucial importance in alteration of the local vasculature to allow penetration into the tissues by antigen-specific T cells, that arrive and interact with local antigen-presenting cells that present relevant peptides of antigens, causing release of cytokines by the T cells, to mediate local inflammation and allergy, or in contrast, immune protection and resistance.

Our current work is seeking to link these basic findings in mice with conditions in humans (asthma, atopic dermatitis), and to dissect out our recent discovery that serum complement components, a system of more than 9 labile enzymatic and fragmenting proteins in the blood, also participate in these critical interactions leading to T cell recruitment in cell mediated immunity in vivo.

Relevant Publications

  • Thomas MJ, Noble A, Sawicka E, Askenase PW, Kemeny DM. CD8 T cells inhibit IgE via dendritic cell IL-12 induction that promotes Th1 T cell counter-regulation. J Immunol. 2002 Jan 1;168(1):216-23.
  • Geba GP, Ptak W, Askenase PW. Topical tacrolimus and cyclosporin A differentially inhibit early and late effector phases of cutaneous delayed-type and immunoglobulin E hypersensitivity. Immunology. 2001 Oct;104(2):235-42.
  • Askenase PW. Yes T cells, but three different T cells (alphabeta, gammadelta and NK T cells), and also B-1 cells mediate contact sensitivity. Clin Exp Immunol. 2001 Sep;125(3):345-50.
  • Thomas MJ, MacAry PA, Noble A, Askenase PW, Kemeny DM. T cytotoxic 1 and T cytotoxic 2 CD8 T cells both inhibit IgE responses. Int Arch Allergy Immunol. 2001 Jan-Mar;124(1-3):187-9.
  • Askenase PW, Tsuji RF. B-1 B cell IgM antibody initiates T cell elicitation of contact sensitivity. Curr Top Microbiol Immunol. 2000;252:171-7.
  • Huang TJ, MacAry PA, Eynott P, Moussavi A, Daniel KC, Askenase PW, Kemeny DM, Chung KF. Allergen-specific Th1 cells counteract efferent Th2 cell-dependent bronchial
    hyperresponsiveness and eosinophilic inflammation partly via IFN-gamma. J Immunol. 2001 Jan 1;166(1):207-17.
  • Heinemann A, Hartnell A, Stubbs VE, Murakami K, Soler D, LaRosa G, Askenase PW, Williams TJ, Sabroe I.
    Basophil responses to chemokines are regulated by both sequential and cooperative receptor signaling. J Immunol. 2000 Dec 15;165(12):7224-33.
  • Hong L, Wackers F, Dewar M, Kashgarian M, Askenase PW.
    Atypical fatal hypocomplementemic urticarial vasculitis with involvement of native and homograft aortic valves in an African American man. J Allergy Clin Immunol. 2000 Dec;106(6):1196-8.
  • Szczepanik M, Askenase PW. IL-12 reverses established tolerance mediated by TCRalphabeta+ but not by TCRgammadelta+ suppressor T cells. Immunol Invest. 2000 Aug;29(3):243-56.
  • Tsuji RF, Kawikova I, Ramabhadran R, Akahira-Azuma M, Taub D, Hugli TE, Gerard C, Askenase PW. Early local generation of C5a initiates the elicitation of contact sensitivity by leading to early T cell recruitment. J Immunol. 2000 Aug 1;165(3):1588-98.

 

Contact

Campus Address
TAC S-215

Mailing Address
333 Cedar St.
New Haven, CT 06510

E-mail
philip.askenase@yale.edu

Office Phone
(203) 785-4143

Fax
(203) 785-3229