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

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T. K. Kondratieva¹, I. A. Linge¹, E. V. Kondratieva¹, A. V. Dyatlov^1,2, M. S. Drutskaya^2,3, R. V. Zvartsev³, S. A. Nedospasov^2,3, and A. S. Apt^1,2*

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

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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.

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KEY WORDS: mycobacterial infections, B-lymphocytes, TNF, lung pathology, mouse models

DOI: 10.1134/S0006297914120098

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