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Perl, T.
B-cell immune responses and body fat topography in immunocompromised and healthy individuals
Humanmedizin; [ Diplomarbeit ] Medizinische Universität Graz; 2023. pp. 62 [OPEN ACCESS]
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Authors Med Uni Graz:
Advisor:
Fessler Johannes
Lackner Sonja
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Abstract:
Introduction: It is well known that obesity has many health disadvantages. Among other things, it leads to chronic low-grade inflammation, which affects the immune system. In this study, we investigated whether and to what extent the amount and distribution of subcutaneous body fat also affects the B-cell immune response. In addition, a connection with the presence of the ACE2 receptor is sought, which is increasingly expressed in body fat and is used by SARS-CoV-2 to enter the cell. Methods: Data was collected as part of the CoVVac study at the Medical University of Graz, which focused on antibody production following Covid-19 vaccination. A cohort of immunocompromised patients (n= 64) and healthy controls (HC group, n= 72) was included in the study. The group of immunocompromised patients was divided into individuals with primary immunodeficiency (PID group, n= 24) and individuals with secondary immunodeficiency (SID group, n=40). The PID group included individuals with genetic immunodeficiencies, and the SID group included people who received B-cell-depleting therapy due to hematologic malignancies, immunosuppressive therapies, or hematopoietic stem cell transplantation. As part of the study, ultrasound measurements of subcutaneous adipose tissue were also performed. In addition, antibodies were determined using an immunoassay and ACE2 levels were measured using the Human ACE2 ELISA Kit from ThermoFisher Scientific. SPSS was used for all calculations between antibodies formed, age, gender, ACE2 levels and body fat distribution. The distribution was calculated with the Shapiro-Wilk test, and group comparisons were calculated with the Mann-Whitney U test. For correlations, the Spearman correlation coefficient was determined.   Results: Significant differences in the number of antibodies formed were observed between the groups. While in the healthy control group all reached a high titer (Md= 2500 U/ml), the median Roche anti-RBD was significantly lower in both the PID group (Md= 1572 U/ml, p =<0.001), and the SID group (Md= 0 U/ml, p =<0.001) compared to the healthy control group. No age or gender differences were found in the antibodies formed. In the healthy control group, there was a significant relationship between age and BMI (p=0.032, r=0.254) and between age and waist circumference (p=0.014, r=0.288). A significant difference in body fat between men and women was found in all groups. In the PGD group, there was a significant correlation between antibodies formed and total body fat (p=0.004, r=0.433), and between antibodies formed and subcutaneous fat measured at the calf (p=0.03, r= 0.462). No correlation with age, fat distribution or gender was found for ACE 2 levels, but gender comparison showed that males had significantly more ACE2 receptors than females (p=0.039). Conclusion: Individuals with immunodeficiency differ both in the amount of body fat and in the number of antibodies formed after vaccination. However, an association between body fat and immune response could only be found in the group of individuals with primary immunodeficiency. Here, people with higher fat mass formed more antibodies than people with less body fat. For the other groups studied, a homogeneous B-cell response was observed with different age and body fat distribution, which is why no influence of body fat mass can be assumed in this cohort.

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