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Linda L. Baum, PhD

Degrees and Certifications:
PhD

Rank and Title:
Associate Professor

Department:
Immunology/Microbiology

Endowed Professorship:

Office Location:
1735 W. Harrison St.
Cohn Building
Room 620
Chicago, IL 60612

Laboratory Location:
1735 W. Harrison St.
Cohn Building
Room 620
Chicago, IL 60612

Phone:
312-942-2881

Fax:
312-942-2808

E-mail:
Linda_L_Baum@rush.edu

Education:
University of Kansas, Lawrence, Kansas
B.A. with Honors in Microbiology, 1971

Michigan State University, East Lansing, Michigan
Ph.D., Microbiology and Public Health, Cellular Immunology, 1976

University of Alberta, Edmonton, Alberta, Canada
Department of Immunology
NIH Postdoctoral Fellowship, Cellular Immunology, 1996-1978

Research Areas:
Biological Phenomena Cell Phenomena and Immunity
Immune System Diseases
Virus Diseases

Laboratory Techniques:

Hyperlinks:

Documents:

Faculty/Staff Description:
The immune defense system is ultimately unable to eliminate HIV from an infected individual, but it is responsible for prolonging the onset of AIDS. Several immune effector mechanisms contribute to defense against HIV disease progression. We are studying antibody dependent cell-mediated cytotoxicity (ADCC). In ADCC, effector cells bind to FcReceptors of HIV specific antibody bound to virus infected cells. ADCC effectors include natural killer cells, monocytes and neutrophils. Our goal is to determine the contribution of ADCC antibodies in host defense against HIV. We compared the titers of ADCC antibodies (anti-HIV gp120) in the cervical lavage fluid of HIV infected women with ADCC antibodies in the serum of women who were part of the Division of AIDS Treatment and Research Initiative (DATRI 009). We demonstrated that: (1) Most HIV infected women have HIV specific ADCC antibody in their serum. Approximately half of these have activity in their CVL. (2) Those women who had HIV specific CVL ADCC titers had significantly lower genital HIV-1 RNA loads even though there was no observable difference in CD4 cell numbers or plasma viral load, suggesting that CVL ADCC may contribute to lower genital viral loads. (3) ADCC activity against HIV-1 in the CVL is mediated by IgG, not by IgA and (4) Caucasian women are more likely to have CVL ADCC antibodies than African American or Latino women. Lower CVL ADCC activity could contribute to greater susceptibility to HIV in African American and Latino women. We are currently looking at the possibility that ADCC against Human Papilloma Virus (HPV) may contribute to the ability of new HPV vaccines to prevent cervical cancer.

Selected Publications:
1. Kim JS, Nag P, Landay AL, Alves A, Cohen M, Bremer JW and Baum LL. Saliva can mediate HIV-1-specific antibody-dependent cell-mediated cytotoxicity. FEMS Immunol Med Microbiol 2006;48:267-73.

2. Martinson JA, Tenorio AR, Montoya CJ, Al-Harthi L, Gichinga CN, Krieg AM, Baum LL and Landay LL. Impact of class A, B and C CpG-ODN on in vitro activation of innate immune cells in HIV-1 infected individuals. Immunology, 2006, in press.

3. Nag P, Kim J, Sapiega V, Landay LL, Bremer JW, Mestecky J, Reichelderfer P, Kovacs A, Cohn J, Weiser B and Baum LL. Women with cervicovaginal antibody-dependent cell-mediated cytotoxicity have lower genital HIV-1 RNA loads. J Infect Dis 2004;190:1970-8.

4. Battle-Miller K, Eby CA, Landay AL, Cohen MH, Sha BE and Baum LL. Antibody-dependent cell-mediated cytotoxicity in cervical lavage fluids of human immunodeficiency virus type 1-infected women. J Infect Dis 2002;185:439-47.

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