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Faculty Detail Faculty Entry   
Name HARRY W SCHROEDER, JR  
Campus Address SHEL 405 Zip 2182
Phone 205-934-4769
E-mail hwsj@uab.edu" id="FacultyDetail1EmailAddress"><a href="mailto:hwsj@uab.edu">hwsj@uab.edu</a>
URL
 
 

Department Affiliations(s)
Appointment Type Department Division Rank
Center  Arthritis & Musculoskeletal Diseases Center  Arthritis & Musculoskeletal Diseases Center Professor
Center  Center for Aging  Center for Aging Professor
Center  Center for AIDS Research  Center for AIDS Research Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Professor
Center  General Clinical Research Center  Ctr for Clinical & Translational Sci Professor
Primary  Medicine  Med - Immunology/Rheumatology Professor
Secondary  Genetics   Genetics Chair Office Professor
Secondary  Microbiology  Microbiology Professor

Biographical Sketch 
Harry W. Schroeder, Jr. (b. 1952), Professor, completed his undergraduate studies in Chemistry (B.S., 1974) at Texas A&M University (College Station, TX). He earned his M.D. (1981) and Ph.D. (1979) with Dr. Bert O'Malley at Baylor College of Medicine (Houston, TX). After completing an Internal Medicine residency at the University of Kentucky (Lexington, KY) in 1984, he trained in Clinical Genetics with Dr. Arno Motulsky at the University of Washington (Seattle, WA), and in molecular immunology with Dr. Roger Perlmutter at the Howard Hughes Medical Institute (Seattle, WA). He was recruited to UAB in 1988 where he has continued to pursue interests in the genetics of diseases of immune function. In 1995-1996, he spent a sabbatical year in the laboratory of Dr. Klaus Rajewsky at the Institute for Genetics of the University of Cologne (Cologne, Germany).

Society Memberships
Organization Name Position Held Org Link
No records
 

Research/Clinical Interest
Title
The Development and Function of Lymphocyte Antigen Receptors. &Genetics of Primary Immune Deficiency Diseases
Description
Although at first glance the power of the mechanisms used to diversify the B- and T-cell antigen receptors appear generate repertoires of random diversity, closer examination reveals striking constraints that are preserved across evolution. The implication is that violation of these constraints programs could lead to immune dysfunction, and thus to disease. Dr. Schroeders group has shown that immunoglobulins belonging to categories outside these constraints are progressive eliminated during development. He has used cre-loxP gene targeting to generate mice wherein the DH locus has been altered to force expression of polyclonal antibody repertoires that lie outside these normal constraints. In these mice, B cell numbers are reduced, responses to T-independent antigens decline in a co-dominant manner, responses to T-dependent antigens and autoantigens are affected in a dominant manner, and autoantibodies can be detected at a very young age. The mechanisms that regulate the normally regulate the repertoire the contribution of violations of these constraints to the development of disease, including autoimmune disorders, are a major focus of the laboratory.
A second focus in the laboratory is the use of classic reverse genetics techniques to elucidate the mechanisms that underlie the development of common variable immune deficiency, the most common primary immune deficiency under the care of clinical immunologists.

Postdoc Positions Available
Date Posted Position Title
No records
 

Selected Publications 
Publication PUBMEDID
Nguyen HH, Zemlin M, Vu HL, Ivanov II, Andrasi J, Zemlin C, Schelonka RL, Schroeder HW Jr, Mestecky J. (2007) Heterosubtypic immunity to influenza A virus infection requires a properly diversified antibody repertoire. J Virol 81:9331-9338.  17567700 
Li J, Cowden LG, King JD, Briles DA, Schroeder HW Jr, Stevens AB, Perry RT, Chen Z, Simmons MS, Wiender HW, Tiwari H, Harrell LE, Go RCP. (2007) Effects of chronic stress and interleukin-10 polymorphisms on antibody response to tetanus vaccine in family caregivers of patients with Alzheimers Disease. Psychosom Med 69:551-559.   17634568 
Schelonka RL, Tanner J, Zhuang Y, Gartland GL, Zemlin M, Schroeder HW Jr. (2007) Categorical selection of the antibody repertoire in splenic B cells. Eur J Immunol 37(4):1010-1021.   17345580  
Johnston DT, Schroeder HW Jr. (2007) B-cell numbers in the blood of patients with non-HLA*B8 or non-HLA*B44 common variable immunodeficiency. Ann Allergy Asthma Immunol. 98(2):163-167.  17304884 
Ippolito, GC, Schelonka RL, Zemlin M, Ivanov I, Kobayashi R, Zemlin C, Gartland L, Nitschke L, Pelkonnen J, Fujihashi K, Rajewsky K, Schroeder HW Jr. (2006) Forced use of an immunoglobulin DH encoding positively charged amino acids impairs B cell development and function. J Exp Med. 203:1567-1578.  16754718 
Johnston DT, Mehaffey G, Thomas J, Young KR Jr, Wiener H, Li J, Li J, Go RCP, Schroeder HW Jr. (2006) Increased frequency of HLA *B44 in recurrent sinopulmonary infections (RESPI). Clin Immunol 119:346-350.  16542878 
Shu H-C, Scot DK, Zhang P, Zhou J, Yang PA, Wu Q, Schroeder HW Jr, Gerald LB, Ravussin E, Jazwinski MS, Mountz JD. (2006) CD8 T-cell immune phenotype of successful aging. Mech Aging Develop 127:231-239.  16313945 
Schelonka RL, Ivanov II, Jung D, Ippolito GC, Nitschke L, Zhuang Y, Gartland GL, Pelkonen J, Alt F, Rajewsky K, Schroeder HW Jr. (2005) A single DH gene segment is sufficient for B cell development and immune function. J Immunol 175:6624-6632.  16272317 
Ivanov II, Schelonka RL, Zhuang Y, Gartland GL, Zemlin M, Schroeder HW Jr. (2005) Development of the expressed immunoglobulin CDR-H3 repertoire is marked by focusing of constraints in length, amino acid utilization, and charge that are first established in early B cell progenitors. J Immunol 174,7773-7780.  15944280 
Link JM, Larson JE, Schroeder HW Jr. (2005) Despite extensive similarity in germline DH and JH sequence, the adult Rhesus macaque CDR-H3 repertoire differs from human. Mol Immunol 42:943-955  15829286 
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Keywords
Common Variable Immune Deficiency, Hypogammaglobulinemia, Antibody Repertoire, B cell Development, TCR repertoire, T cell development, Systemic Lupus Erythematosus, Mouse Models of Autoimmune Disease

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