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Formation of Compact Aggregates of B-lymphocytes in Lung Tissue during Mycobacterial Infection in Mice Depends on TNF Production by These Cells and Is Not an Element of the Host’s Immunological Protection

T. K. Kondratieva1, I. A. Linge1, E. V. Kondratieva1, A. V. Dyatlov1,2, M. S. Drutskaya2,3, R. V. Zvartsev3, S. A. Nedospasov2,3, and A. S. Apt1,2*

1Central Research Institute of Tuberculosis, Russian Academy of Medical Sciences, Yauzskaya Alley 2, 107564 Moscow, Russia; E-mail: asapt@aha.ru

2Lomonosov Moscow State University, Biology Faculty, 119991 Moscow, Russia

3Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, ul. Vavilova 32, 119991 Moscow, Russia; fax: +7 (499) 135-1405; E-mail: isinfo@eimb.ru

* To whom correspondence should be addressed.

Received May 14, 2014; Revision received June 9, 2014
Tumor necrosis factor (TNF) plays a pivotal role in the early control of Mycobacterium tuberculosis and M. avium infections by a host. It was previously shown that both phagocyte-derived and T-cell-derived TNF productions are critical for protective immunity against M. tuberculosis, but the role of TNF produced by B-cells remained unclear. By comparing mice with B-cell-specific TNF deletion to littermate control mice, here we show that TNF production by B-lymphocytes is essential for the formation of infection-specific aggregates of B-cells in the lung. It is likely that these compact foci represent a pathogenic feature of inflammatory response rather than an element of protective immunity, since the capacity to form aggregates has no influence on the severity of M. tuberculosis- and M. avium-triggered diseases.
KEY WORDS: mycobacterial infections, B-lymphocytes, TNF, lung pathology, mouse models

DOI: 10.1134/S0006297914120098