BEGIN:VCALENDAR
VERSION:2.0
PRODID:icalendar-ruby
CALSCALE:GREGORIAN
X-WR-CALNAME:Biomolecular Sciences Seminar Series - Dr. Chih-Ming Tsai
X-WR-TIMEZONE:Mountain Time (US & Canada)
BEGIN:VEVENT
DTSTAMP:20260907T061907Z
UID:tag:localist.com\,2008:EventInstance_50755330635068
DTSTART:20251001T090000Z
DTEND:20251001T221500Z
DESCRIPTION:Biomolecular Sciences Seminar Series \n\nDr. Chih-Ming Tsai\n\n
 Title:  Immune Imprinting as the Basis for Staphylococcal Vaccine Failures
 \n\nAbstract: Staphylococcus aureus (SA) navigates a dual role as both a s
 ymbiont and an occasional deadly pathogen\, yet no successful vaccines exi
 st to combat SA infection in humans. Although exposure to SA in both human
  and mouse generates robust anti-SA antibodies (anti-SA Ab)\, these antibo
 dies only provide modest or no significant protection against SA infection
 . Recently\, we identified the reasons behind the failure of all clinical 
 SA vaccines. Our research demonstrated that prior SA-exposed mice develop 
 anti-SA Ab with shifted epitopes and increased Fc sialylation\, which are 
 ineffective in supporting the killing of pathogens both in vitro and in vi
 vo. Staphylococcal vaccination in prior SA-exposed mice recalls this non-p
 rotective immune imprint\, thereby interfering with vaccine efficacy. Mech
 anistically\, IL-10–secreting B10 cells suppress both recalled and de no
 vo B cell responses. IL-10 promotes STAT3 binding upstream of the sialyltr
 ansferase gene st3gal4\, increasing B cell expression and hyper–α2\,3-s
 ialylation of antibodies. This modification diminishes the protective acti
 vity of antibodies targeting cell-wall antigens IsdB\, IsdA\, and MntC. Co
 nsistent with these findings\, human anti-SA antibodies and anti-Pseudomon
 as antibodies from cystic fibrosis patients with elevated IL-10 show simil
 ar hyper-sialylation compared to antibodies from healthy controls. These r
 esults reveal a pathobiont-driven mechanism whereby IL-10–mediated antib
 ody glycosylation rewires humoral immunity\, providing a mechanistic expla
 nation for vaccine failure and a potential barrier to effective staphyloco
 ccal vaccination.\n\n \n\nHost: Dr. Julie Tinker
GEO:43.606007;-116.206294
LOCATION:Education Building (EDUC)\, 109
SUMMARY:Biomolecular Sciences Seminar Series - Dr. Chih-Ming Tsai
URL;VALUE=URI:https://events.boisestate.edu/event/biomolecular-sciences-sem
 inar-series-dr-chih-ming-tsai
CATEGORIES:Lectures and Presentations
END:VEVENT
BEGIN:VEVENT
DTSTAMP:20260907T061907Z
UID:tag:localist.com\,2008:EventInstance_50756121914969
DTSTART:20251001T210000Z
DTEND:20251001T221500Z
DESCRIPTION:Biomolecular Sciences Seminar Series \n\nDr. Chih-Ming Tsai\n\n
 Title:  Immune Imprinting as the Basis for Staphylococcal Vaccine Failures
 \n\nAbstract: Staphylococcus aureus (SA) navigates a dual role as both a s
 ymbiont and an occasional deadly pathogen\, yet no successful vaccines exi
 st to combat SA infection in humans. Although exposure to SA in both human
  and mouse generates robust anti-SA antibodies (anti-SA Ab)\, these antibo
 dies only provide modest or no significant protection against SA infection
 . Recently\, we identified the reasons behind the failure of all clinical 
 SA vaccines. Our research demonstrated that prior SA-exposed mice develop 
 anti-SA Ab with shifted epitopes and increased Fc sialylation\, which are 
 ineffective in supporting the killing of pathogens both in vitro and in vi
 vo. Staphylococcal vaccination in prior SA-exposed mice recalls this non-p
 rotective immune imprint\, thereby interfering with vaccine efficacy. Mech
 anistically\, IL-10–secreting B10 cells suppress both recalled and de no
 vo B cell responses. IL-10 promotes STAT3 binding upstream of the sialyltr
 ansferase gene st3gal4\, increasing B cell expression and hyper–α2\,3-s
 ialylation of antibodies. This modification diminishes the protective acti
 vity of antibodies targeting cell-wall antigens IsdB\, IsdA\, and MntC. Co
 nsistent with these findings\, human anti-SA antibodies and anti-Pseudomon
 as antibodies from cystic fibrosis patients with elevated IL-10 show simil
 ar hyper-sialylation compared to antibodies from healthy controls. These r
 esults reveal a pathobiont-driven mechanism whereby IL-10–mediated antib
 ody glycosylation rewires humoral immunity\, providing a mechanistic expla
 nation for vaccine failure and a potential barrier to effective staphyloco
 ccal vaccination.\n\n \n\nHost: Dr. Julie Tinker
GEO:43.606007;-116.206294
LOCATION:Education Building (EDUC)\, 109
SUMMARY:Biomolecular Sciences Seminar Series - Dr. Chih-Ming Tsai
URL;VALUE=URI:https://events.boisestate.edu/event/biomolecular-sciences-sem
 inar-series-dr-chih-ming-tsai
CATEGORIES:Lectures and Presentations
END:VEVENT
END:VCALENDAR