Avaliação imunológica nas pregas vestibulares de pacientes autopsiados com a Síndrome da Imunodeficiência Adquirida

Abstract

Em pacientes com Síndrome da Imunodeficiência Adquirida há uma diminuição das células envolvidas na resposta imune, o que influencia na população celular dos folículos linfóides encontrados nas pregas vestibulares, favorecendo o aparecimento de infecções nas vias aéreas destes pacientes. Estas infecções são a principal causa de mortalidade e morbidade nestes pacientes. OBJETIVO: Caracterizar a população de células nos folículos linfóides localizados nas pregas vestibulares de adultos autopsiados com Síndrome da Imunodeficiência Adquirida, com e sem infecções respiratórias associadas. MATERIAIS E MÉTODOS: Foi realizado um estudo retrospectivo transversal em 64 laringes de adultos coletadas na rotina das autopsias. Para a imunohistoquímica foram utilizados os anticorpos: Anti-B cells, Anti-CD3, Anti-CD68 e Anti-follicular dendritic cells. RESULTADOS: 46 (71,87%) dos pacientes estudados tinham diagnóstico de Síndrome da Imunodeficiência Adquirida. Nestes pacientes, a celularidade dos folículos linfóides foi estatisticamente menor em relação ao grupo controle em todos os fenótipos estudados. Nos pacientes imunodeprimidos com infecção respiratória associada, o número de células estava diminuído, sendo significante no caso dos linfócitos T (p=0,024). CONCLUSÃO: Em nosso estudo demonstramos que os folículos linfóides das pregas vestibulares são afetados pela infecção viral e representam com fidedignidade o estado imunológico de imunodepressão destes pacientes.

Mucosa-associated lymphoid tissue in individuals with AIDS

“…The slides were then washed with distilled water, counterstained with hematoxylin and mounted in entellan. For the morphometric analysis of false vocal fold lymphoid follicle cells, immunohistochemistry was done for B and T lymphocytes, macrophages, and follicular dendritic cells; primary anti-B-cells (Biogenex, 1:100), anti-CD3 (Dako, 1:40), anti-CD68 (Dako, 1:80), and anti-follicular dendritic cells (Dako, 1:80) 5 antibodies were used. The following antibodies were used for evaluating the immunoglobulins: anti-IgA (Novocastra ® , 1:1000), Anti-IgG (Novocastra ® , 1:1000), and anti-IgM (Novocastra ® , 1:800).…”

“…Other immune cells could harbor the virus, and thus lymphoid tissues, such as those in the larynx, were perceived as possible viral replication structures. [2][3][4][5] Lymphoid follicles result from the union of different types of B and T lymphocytes; when close to mucosae, they produce substances that active the local immune response against infectious agents. Lymphoid follicles located in vestibular folds (two thick sagittally oriented laminae, with a double-sized mucosa, that arises within the supraglottic wall) 6 protect upper airways, similarly to lymphoid tissues associated with mucosae.…”

“…[21][22][23][24] Studies done in our department have demonstrated the nature of cells composing the lymphoid follicles in vestibular folds of adults 9 and their depletion in AIDS cases. 5 Because of the importance of the immune system for local protection of mucosae, knowing the composition, arrangement and function of lymphoid follicles in vestibular folds is the first step in understanding the mechanisms involved in respiratory infection in AIDS patients. Thus, the purpose of this study was to assess the effect of fibrosis on the architecture of lymphoid follicles in the vestibular folds of autopsied AIDS adults, and to assess their function by quantifying the immunoglobulins produced in these follicles.…”

“…Other immune cells could harbor the virus, and thus lymphoid tissues, such as those in the larynx, were perceived as possible viral replication structures. 2 , 3 , 4 , 5 …”

“… 10 , 11 , 12 Cytokines produced in lymphoid follicles cause plasmacytic differentiation and antibody production (mostly IgA in the respiratory tract), a component of mucosal cell secretions, including that of the vestibular folds. 5 , 13 Cell-mediated and humoral immunity are unable to control infection in HIV-positive subjects, resulting in loss of several lymphocyte functions and increased susceptibility to secondary and opportunistic infection. Part of the immune dysfunction is in polyclonal B lymphocytes; these are constantly activated, which may result in spontaneous hypergammaglobulinemia.…”