Endowed Professor in Lung Immunology

Assistant Dean for Research Administration, School of Medicine and Office of the Senior Vice Provost

Division of Pulmonary, Allergy & Critical Care Medicine
1900 University Blvd., THT-422
University of Alabama at Birmingham
Birmingham, AL 35294

Contact Information


Campus Address:


 THT 422

Academic Office location:


 THT 429-A

Office Phone:


 (205) 996-9598

Office Fax (Academic):


 (205) 934-1721

Email Address:



Lab Assistant:  
Jonathan Blackburn
Ph: (205) 996-9599 

Fax: (205) 934-1721  

Brief Bio
Dr. Claude H. (Chad) Steele III was born in Pensacola, Florida in 1972 and his family moved to northeast Louisiana the following year. Dr. Steele attended the University of Louisiana at Monroe (formerly Northeast Louisiana University), receiving a Bachelor's degree in Chemistry in 1995. After an 18 month stint as an industrial chemist, Dr. Steele entered graduate school in the Department of Microbiology at Louisiana State University Health Sciences Center-New Orleans, earning a Masters degree in December 1998, followed by a Doctorate in December 2000, both under the mentorship of Dr. Paul Fidel. Dr. Steele remained at LSUHSC for his post-doctoral fellowship, conducting lung host defense research in the laboratories of Dr. Jay Kolls and Dr. Judd Shellito. In July 2003, Dr. Steele was recruited as faculty to the Department of Pediatrics at the University of Pittsburgh, where he remained until June 2007. In July 2007, Dr. Steele was recruited to join the faculty at the University of Alabama at Birmingham, in the Division of Pulmonary, Allergy & Critical Care Medicine, where he is currently a tenured Professor of Medicine.

Research Interests
Research in Dr. Steele's Laboratory of Lung Immunology and Host Defense is focused on understanding innate and adaptive immune responses against opportunistic fungal pathogens that cause life-threatening lung infections in immunocompromised individuals with such diseases as HIV, COPD and leukemia. Dr. Steele's research on the fungal pathogen Pneumocystis carinii has uncovered a role for alternative macrophage activation, termed M2a, that is associated with more efficient elimination of P. carinii from the lungs. Dr. Steele's lab is currently characterizing multiple M2a-associated innate host defense molecules in an effort to understand what influences alveolar macrophage effector responses against P. carinii. In a new project, Dr. Steele’s lab is investigating how Th2 responses are generated during P. carinii lung infection and how B cells affect the CD4 T cell phenotype during infection. In other projects, Dr. Steele's research team has discovered an essential role for a myeloid-associated fungal recognition receptor, Dectin-1, in lung innate immune responses to the fungal pathogen Aspergillus fumigatus. Dectin-1, which recognizes beta-glucan carbohydrates found in the cell wall of all medically-important fungi, controls the production of multiple inflammatory cytokines, including IL-17A and IL-22. In invasive aspergillosis (IA), Dr. Steele’s lab has shown that IL-17A and IL-22 are required for protection against infection, yet during A. fumigatus-associated asthma (AFAA), IL-17A and IL-22 function in an immunopathogenic role and contributes to asthma severity. Dr. Steele's lab is currently focusing on the lung cell sources of IL-17A and IL-22 during IA and AFAA, which pathways drive the development of these cell populations and the downstream IL-17A- and IL-22-associated mechanisms that promote elimination of A. fumigatus from the lungs vs. those driving deleterious responses during fungal asthma.

Key Publications
Lilly, L.M., M.A. Gessner, C.W. Dunaway, A.E. Metz, L.M. Schwiebert, C.T. Weaver, G.D. Brown and C. Steele. The beta-glucan receptor Dectin-1 promotes immunopathology during fungal allergy via IL-22. Journal of Immunology 189(7):3653-60. (2012) PMID:22933634

Nelson, M.P., B.S. Christmann, A. Burg, C. Dunaway, A. Morris and C. Steele. Experimental Pneumocystis lung infection promotes M2a alveolar macrophage-derived MMP12 production. American Journal of Physiology – Lung Cellular and Molecular Physiology 303:L469-75 (2012) PMID:22773692

Gessner, M.A., S. Doran, Z. Yu, C.W. Dunaway, S. Matalon and C. Steele. Chlorine gas exposure increases susceptibility to invasive lung fungal infection. American Journal of Physiology – Lung Cellular and Molecular Physiology 304:L765-73 (2013). PMID:23564508

Myers, R., C. W. Dunaway, M.P. Nelson, J.L. Trevor, A. Morris and C. Steele. STAT4-dependent and -independent T helper type 2-mediated immunity mediates protection against lung infection with Pneumocystis murina. Journal of Immunology 190(12):6287-94 (2013). PMID:23650614

Lilly, L.M., M.P. Nelson, A.R. Burg, C.W. Dunaway and C. Steele. Eosinophil deficiency compromises lung defense against Aspergillus fumigatus. Infection and Immunity 82:1315-25 (2014). PMID: 24379296

Werner, J.L. and C. Steele. Innate receptors and cellular defense against pulmonary infections. Journal of Immunology 193(8):3842-50 (2014). PMID: 25281754

Please click here to see Dr. Steele's complete publications listing.

SOM Epilogue Menu