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Separation of Immune Cell Subpopulations in Peripheral Blood Samples from Children with Infectious Mononucleosis
Published on: September 7, 2022
Peripheral blood monocyte and T cell subsets in children with specific polysaccharide antibody deficiency (SPAD)
1Immunology Department, IMEX-CONICET-Academia Nacional de Medicina, Buenos Aires, Argentina.
Abstract:
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.
Insights
Specific polysaccharide antibody deficiency (SPAD) involves more than just B cell defects. This study found immune cell alterations in SPAD patients, suggesting a more complex immunodeficiency than previously understood.
Area of Science:
- Immunology
- Clinical Medicine
Background:
- Specific polysaccharide antibody deficiency (SPAD) is an immunodeficiency marked by poor antibody production against encapsulated bacteria like Streptococcus pneumoniae.
- Previous understanding suggested SPAD primarily involved B cell defects, sufficient to explain recurrent infections.
Purpose of the Study:
- To investigate if SPAD patients exhibit defects in leukocyte subpopulations beyond B cells.
- To determine if these additional defects contribute to impaired adaptive immunity against Streptococcus pneumoniae.
Main Methods:
- Analysis of leukocyte subpopulations in SPAD patients.
- Flow cytometry to assess monocyte subsets (CD14++ CD16-, CD14++ CD16+) and T cell populations.
Main Results:
- SPAD patients lack the typical age-related changes in monocyte percentages seen in healthy children.
- Absence of increased classical monocytes (CD14++ CD16-) and decreased intermediate monocytes (CD14++ CD16+) with age.
- Observed alterations in T cell populations within SPAD patients.
Conclusions:
- The immune deficiency in SPAD patients is more complex than previously recognized, extending beyond B cell dysfunction.
- Defects in monocytes and T cells may contribute to the recurrent infections observed in SPAD.
- Further research is needed to fully elucidate the multifaceted immune dysregulation in SPAD.
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