Peripheral blood monocyte and T cell subsets in children with specific polysaccharide antibody deficiency (SPAD)

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• 作者：C. Otero^a ; D. Dí ; az^b ; I. Uriarte^b ; L. Bezrodnik^b ; M.R. Finiasz^a ; ¹ ; S. Fink^a ; ¹ ; ^{sfink@hematologia.anm.edu.ar" class="auth_mail" title="E-mail the corresponding author} ; ^{finksusana@gmail.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Primary immunodeficiency ; Pneumococcus ; Monocytes ; T cells ; Cell activation ; Cytokines
• 刊名：Human Immunology
• 出版年：2016
• 出版时间：January 2016
• 年：2016
• 卷：77
• 期：1
• 页码：12-19
• 全文大小：1122 K

文摘

Specific polysaccharide antibody deficiency (SPAD) is a well reported immunodeficiency characterized by a failure to produce antibodies against polyvalent polysaccharide antigens, expressed by encapsulated microorganisms. The clinical presentation of these patients involves recurrent bacterial infections, being the most frequent agent Streptococcus (S.) pneumoniae. In SPAD patients few reports refer to cells other than B cells. Since the immune response to S. pneumoniae and other encapsulated bacteria was historically considered restricted to B cells, the antibody deficiency seemed enough to justify the repetitive infections in SPAD patients. Our purpose is to determine if the B cell defects reported in SPAD patients are accompanied by defects in other leukocyte subpopulations necessary for the development of a proper adaptive immune response against S. pneumoniae. We here report that age related changes observed in healthy children involving increased percentages of classical monocytes (CD14++ CD16− cells) and decreased intermediate monocytes (CD14++ CD16+ cells), are absent in SPAD patients. Alterations can also be observed in T cells, supporting that the immune deficiency in SPAD patients is more complex than what has been described up to now.