Cycle dependent RCAS1 expression with respect to the immune cells presence and activity.
BACKGROUND
The number of cytotoxic immune cells grows in the endometrium during the secretory cycle phase. RCAS1 is a protein inhibiting the activated immune cytotoxic cells. The expression of RCAS1 has been confirmed in endometrium. The aim of the present study was to evaluate the RCAS1 expression alterations with respect to the menstrual cycle changes and the number and activity of cytotoxic immune cells.


METHODS
RCAS1, CD25, CD69, CD56, CD16, CD68 antigens expression was assessed by immunohistochemistry in endometrial tissue samples which were obtained from 33 patients. Tissue samples were classified according to the menstrual cycle phases, with division of the cycle into three phases: proliferative (8 cases), periovulatory (10 cases), and secretory (15 cases) ones.


RESULTS
A significantly higher RCAS1 expression was observed in the periovulatory and the secretory menstrual cycle phases than in the proliferative phase. The changes in RCAS1 expression were combined with significant differences in the number of immune cells and their activity. The highest level of CD69 antigen expression was observed during the periovulatory cycle phase, while the highest level of CD25 antigen expression was observed during proliferative phase, the number of CD56 positive cells was at the highest level during the secretory cycle phase. No significant differences in the number of macrophages and CD16 antigen expression were observed with respect to the menstrual cycle phases.


CONCLUSIONS
RCAS1 endometrial expression may favor the coexistence of active lymphocytes and endometrial cells.
Wicherek
Lukasz
L
Department of Gyneacology and Infertility, Jagiellonian University, Krakow, Poland. mowicher@cyf-kr.edu.pl
Klimek
Marek
M
Galazka
Krystyna
K
Obrzut
Bogdan
B
D000328:Adult; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism; D000951:Antigens, Neoplasm / Q000378:metabolism*; D019002:CD56 Antigen / Q000378:metabolism; D004717:Endometrium / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D005260:Female; D058851:GPI-Linked Proteins; D006801:Humans; D007107:Immune System / Q000166:cytology* / Q000378:metabolism*; D007150:Immunohistochemistry; D053645:Interleukin-2 Receptor alpha Subunit / Q000378:metabolism; D037181:Lectins, C-Type; D008597:Menstrual Cycle / Q000276:immunology* / Q000378:metabolism*; D008875:Middle Aged; D017452:Receptors, IgG / Q000378:metabolism; D000099192:CD69 Antigens; D000097382:CD68 Molecule
D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000945:Antigens, Differentiation, T-Lymphocyte; D000951:Antigens, Neoplasm; D019002:CD56 Antigen; D058851:GPI-Linked Proteins; D053645:Interleukin-2 Receptor alpha Subunit; D037181:Lectins, C-Type; D017452:Receptors, IgG; D000099192:CD69 Antigens; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C120762:EBAG9 protein, human; C428200:FCGR3B protein, human