TUMORS HARVESTED FROM LSP1 KO MICE HAVE A LOWER FREQUENCY OF TOTAL LEUCOCYTES DUE TO MIGRATION DEFECTS

MERCEDES PASCUAL; NICOLAS DANIEL DHO; RACHEL ACLAND; MARÍA INÉS CRESPO; MARÍA C PISTORESI- PALENCIA; BELKYS A. MALETTO; GABRIEL MORÓN

San Miguel de Tucumán

Congreso; LXVII Reunión de la Sociedad Argentina de Inmunología; 2019

Sociedad Argentina de Inmunología

Leukocyte-specific protein1 (LSP1) is a 52kDa cytoplasmic F-actin binding phosphoprotein expressed in allhuman and murine leukocytes as well as in endothelial cells. This protein in knownas an important regulator of actin cytoskeleton remodeling. It was reported thatLSP1 polymorphisms or downregulation are considered risk factors for some typesof cancer. We previously shown that tumors in Lsp1-/- mice grew significantly fasterand bigger than in wild type (WT) controls. In order to study the role of LSP1 inantitumor immune response, we employed the B16-OVA melanoma model. WT and Lsp1-/-mice were subcutaneously-injected injected with 105 B16-OVA cells and followed-upuntil day 15. Tumors were analyzed by flow cytometry, showing a lower frequencyof total infiltrating leukocytes (CD45+ cells) in tumors obtained from Lsp1-/- micecompared to their WT counterpart (p<0.01). Nonetheless, the leukocyte subpopulationsproportions were similar in both animal groups. Considering that LSP1 is expressedby leukocytes and endothelial cells, an in vivo migration assay was performed. Weobserved a lower frequency of LSP1 KO migrant leukocytes in tumors developed inLsp1-/- mice but not in WT mice (p<0.05). However, no difference in migrant cellswas found when spleens or tumor draining lymph nodes were analyzed. We hypothesizethat the impaired control of melanoma growth in Lsp1-/- mice could be caused atleast in part, by the lower frequency of total leukocytes in tumor. This event mightbe a result of a reduced extravasation efficiency of Lsp1-/- leukocytes, combinedwith a modified vessels structure.  <!-- /* Font Definitions */ @font-face{font-family:Helvetica;panose-1:0 0 0 0 0 0 0 0 0 0;mso-font-alt:Helvetica;mso-font-charset:0;mso-generic-font-family:auto;mso-font-pitch:variable;mso-font-signature:-536870145 1342208091 0 0 415 0;}@font-face{font-family:"Cambria Math";panose-1:2 4 5 3 5 4 6 3 2 4;mso-font-charset:0;mso-generic-font-family:roman;mso-font-pitch:variable;mso-font-signature:-536870145 1107305727 0 0 415 0;}@font-face{font-family:Calibri;panose-1:2 15 5 2 2 2 4 3 2 4;mso-font-alt:Calibri;mso-font-charset:0;mso-generic-font-family:swiss;mso-font-pitch:variable;mso-font-signature:-536859905 -1073697537 9 0 511 0;}@font-face{font-family:"Times New Roman \(Cuerpo en alfa";panose-1:2 11 6 4 2 2 2 2 2 4;mso-font-alt:"Times New Roman";mso-font-charset:0;mso-generic-font-family:roman;mso-font-pitch:variable;mso-font-signature:-536859921 -1073711039 9 0 511 0;} /* Style Definitions */ p.MsoNormal, li.MsoNormal, div.MsoNormal{mso-style-unhide:no;mso-style-qformat:yes;mso-style-parent:"";margin:0cm;margin-bottom:.0001pt;mso-pagination:widow-orphan;font-size:12.0pt;font-family:Helvetica;mso-fareast-font-family:Calibri;mso-fareast-theme-font:minor-latin;mso-bidi-font-family:"Times New Roman \(Cuerpo en alfa";mso-ansi-language:ES-TRAD;mso-fareast-language:EN-US;}.MsoChpDefault{mso-style-type:export-only;mso-default-props:yes;font-family:Helvetica;mso-ascii-font-family:Helvetica;mso-fareast-font-family:Calibri;mso-fareast-theme-font:minor-latin;mso-hansi-font-family:Helvetica;mso-bidi-font-family:"Times New Roman \(Cuerpo en alfa";mso-ansi-language:ES-TRAD;mso-fareast-language:EN-US;}size:595.0pt 842.0pt;margin:70.85pt 3.0cm 70.85pt 3.0cm;mso-header-margin:35.4pt;mso-footer-margin:35.4pt;mso-paper-source:0;}div.WordSection1{page:WordSection1;}