Anti-CD20 (rituximab) therapy for anti-IFN-γ autoantibody-associated nontuberculous mycobacterial infection

被引:150
作者
Browne, Sarah K. [1 ]
Zaman, Rifat [1 ]
Sampaio, Elizabeth P. [1 ,2 ]
Jutivorakool, Kamonwan [1 ,3 ,4 ]
Rosen, Lindsey B. [1 ]
Ding, Li [1 ]
Pancholi, Minjal J. [1 ]
Yang, Lauren M. [1 ,5 ]
Priel, Debra Long [6 ]
Uzel, Gulbu [1 ]
Freeman, Alexandra F. [1 ]
Hayes, Carlton E. [7 ]
Baxter, Roger [8 ]
Cohen, Stuart H. [9 ]
Holland, Steven M. [1 ]
机构
[1] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA
[2] Fiocruz MS, Inst Oswaldo Cruz, Leprosy Lab, BR-21045900 Rio De Janeiro, Brazil
[3] Chulalongkorn Univ, Fac Med, Dept Med, Bangkok, Thailand
[4] King Chulalongkorn Mem Hosp, Thai Red Cross Soc, Bangkok, Thailand
[5] Washington Univ, Sch Med, St Louis, MO USA
[6] SAIC Frederick Inc, Clin Serv Program, Natl Canc Inst Frederick, Frederick, MD USA
[7] Jackson Clin, Jackson, TN USA
[8] So Calif Permanente Med Grp, Oakland, CA USA
[9] Univ Calif Davis, Dept Epidemiol & Infect Control, Davis, CA 95616 USA
基金
美国国家卫生研究院;
关键词
INTERFERON-GAMMA; RHEUMATOID-ARTHRITIS; PEMPHIGUS-VULGARIS; MYASTHENIA-GRAVIS; AVIUM COMPLEX; PATIENT; INTERLEUKIN-12; AUTOIMMUNITY; RECURRENT; LYMPHOMA;
D O I
10.1182/blood-2011-12-395707
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Patients with anti-IFN-gamma autoantibodies have impaired IFN-gamma signaling, leading to severe disseminated infections with intracellular pathogens, especially nontuberculous mycobacteria. Disease may be severe and progressive, despite aggressive treatment. To address the underlying pathogenic IFN-gamma autoantibodies we used the therapeutic monoclonal rituximab (anti-CD20) to target patient B cells. All subjects received between 8 and 12 doses of rituximab within the first year to maintain disease remission. Subsequent doses were given for relapsed infection. We report 4 patients with refractory disease treated with rituximab who had clinical and laboratory evidence of therapeutic response as determined by clearance of infection, resolution of inflammation, reduction of anti-IFN-gamma autoantibody levels, and improved IFN-gamma signaling. (Blood. 2012;119(17):3933-3939)
引用
收藏
页码:3933 / 3939
页数:7
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