Polly matzinger biography of william

French-born American immunologist

Polly Celine Eveline Matzinger (born July 21, 1947) is a French-born immunologist who proposed the danger model notionally of how the immune silhouette works.^[1]

Early years

Polly Matzinger was by birth on July 21, 1947, be next to France to a French dam (Simone) and a Dutch sire (Hans).^[1] In 1954, she immigrated to the U.S.

with wise sister, Marjolaine, and parents. Restlessness prior jobs included being unadorned bass jazz musician, carpenter, pursue trainer, waitress, and Playboy Bunny.^[2][3] She finished her bachelor's cherished science in biology at glory University of California, Irvine expect 1976,^[3] and doctorate in collection at the University of Calif., San Diego in 1979.^[4][5] She then did four years human postdoctoral work at the Custom of Cambridge^[3] and was clean up scientist at the Basel for Immunology for six majority before working at the State-owned Institutes of Health in Bethesda, Maryland.^[5]

Ghost Lab at NIAID

Matzinger in your right mind chief of the T-Cell Patience and Memory Section at justness U.S.

National Institute of Hypersensitivity and Infectious Diseases (NIAID).^[6] Decency lab has been referred tip off as the "Ghost Lab" ardently desire Matzinger's choice to conduct goodness first nine months of quota research alone with a high point on chaos theory.^{[citation needed]} Lead to 2013, while reorganizing the Lab of Cellular and Molecular Immunology, NIAID transferred Matzinger's section abut the Laboratory of Immunogenetics.^[6]

In 2015, Matzinger recorded an eight-part keep in shape on the danger model criticize the immune system, covering displace rejection, tumors, autoimmunity, T cells, parasites, and alarmins.^[7]

Research

The danger model

The Self/Non-self Model proposed by Macfarlane Burnet and Frank Fenner recovered 1949 faced challenges in decency late 1980s as immunologists certified that T cells depend trumped-up story antigen-presenting cells showcasing materials existing sending co-stimulatory signals.

Driven uncongenial the writings of Thomas Chemist on paradigm shifts in discipline, Charles Janeway made a 1989 proposal that the innate insusceptible system was the real janitor of immune system responses. Fiasco also theorized that the unbeatable immune system used ancient pattern-recognition receptors to make these decisions, recognizing a pathogen by secure unchanging characteristics.^{[citation needed]}

Danger signals

In churn out 1994 article "Tolerance, Danger, stake the Extended Family", Matzinger stretched the danger model, arguing go antigen-presenting cells respond to "danger signals" released from cells undergoing unprogrammed cell death when skinned or stressed, as opposed take it easy apoptosis (controlled cell death).

Representation alarm signals released by these cells let the immune practice know that there is straighten up problem requiring an immune satisfy. She argued that T cells and the immune response they orchestrate occur not because dear a neonatal definition of "self", as in the previous mock-up, nor because of ancient definitions of pathogens, as in Janeway's argument, but because of boss dynamic and constantly updated comment to danger as defined overtake cellular damage.^[8]

Scope

The danger model attempt broad, covering topics as mixed as transplantation, maternal/fetal immunity, autoimmunity, cancer treatments, and vaccines.

Matzinger argued that prior models blundered to explain why immune road responses vary based on excellence specific threat's location and hardness. Prior models also fail give somebody the job of explain how the immune profile rejects tumors, induces autoimmune diseases, or generates allergic responses.

Some immunologists still maintain Janeway's meaning, believing that the immune reply is mainly fueled by aim evolutionarily conserved "pattern recognition receptors" that recognize similarities between bacilli, minimizing the effects of unprogrammed cell death.^{[citation needed]}

Pattern recognition stream a tissue-driven immune system

Seung-Yong Seong and Matzinger have proposed not built up hydrophobic regions on biological compounds as among the damage-associated molecular patterns (DAMPs) of the risk model.

Facing stressors, cells misfold and denature their proteins, exposing hydrophobic regions that aggregate space clumps to avoid exposure hug the water-filled environment.^[9]

In a 2013 article in Nature Immunology, Matzinger highlighted the danger model's main implication that bodily tissues ride immune responses.

As research continues to show the bacteria be useful to each organ's microbiome guiding disloyalty function and outputs, Matzinger theorizes that microbes may be shown as driving immune system responses.^[10] Matzinger argues that DAMPs may well explain why toll-like receptors acknowledge to both external and endogenic ligand signals with her risk model suggesting a multitude help signalling pathways determining the control and nature of each safe system response.

Challenges to Matzinger's theories

Regulatory T cells have back number shown suppressing immune responses, exemplified by the autoimmune IPEX peculiar to occurring when the master watchdog of these T_reg cells commission dysfunctional.^[11] Matzinger has incorporated T_reg cells into her danger conceive, arguing that their regulation action is not absolute, based turn down transplant organs being rejected combination higher rates if infected, presentation that danger signals continue be proof against dictate the immune response.^[12]

Criticisms get the picture the danger model focus form two key points: First, Matzinger argued that tumors persist tongue-lash cause cancer because their cells undergo programmed cell death, devoted to release danger signals promote an immune response.

However, late research has shown the secure system detecting and destroying set on tumors. Second, the danger mould explains transplant rejection as position result of surgery-induced damage, on the other hand this explanation fails to prize for greater tolerance of autotransplantation, the movement of tissue mid parts of the same body.^[13]

Terms coined by Matzinger, such because "professional antigen-presenting-cell", "danger signal", pivotal "DAMPs", are frequently repurposed demand explanations of the self/non-self imitation of the immune system.

Character immunologist Russell E. Vance has argued that immunological paradigms choose the danger model are come what may inaccurate representations of distinct mechanisms generated under evolutionary pressure.^[14]

Dog co-author controversy

In 1978, Matzinger published amass fourth paper in the Journal of Experimental Medicine, listing restlessness Afghan Hound, Galadriel Mirkwood, type a coauthor to write notch a third-person active voice.^[15] Arrive unexpectedly identifying this, she was prohibited from publishing in the journal.^[16]

Awards

At the 1986 Köln Film Commemoration, Polly Matzinger won the Accord for Special Excellence in Didactic Films for the German construction of Immunity: The Inside Story.

In 1996, she was inducted as an honorary lifetime associate of the Scandinavian Society pursuit Immunology. In 2002, Discover munitions dump recognized Matzinger as one objection the fifty most important troop in science.^[17] In 2003, she received an honorary doctorate deseed Hasselt University. In 2008, she was listed as a "Highly Cited" research among the silence 1% of citations for tiara field on the Web depart Science.^[6]

Since 2009, the biotechnology association EpiVax has funded the Polly Matzinger Fearless Scientist Scholarship defend women scientists at the Further education college of Rhode Island's Institute unjustifiable Immunology & Informatics that suppress challenges.^[18]

Publications

• Matzinger P., Mirkwood G.

  (1978). "In a fully H-2 contradictory chimera, T cells of donator origin can respond to smaller histocompatibility antigens in association down either donor or host H-2 type". Journal of Experimental Medicine. 148 (1): 84–92. doi:10.1084/jem.148.1.84. PMC 2184911. PMID 78964.

• Lassila, O., Vainio, O.

  dominant Matzinger, P. (1988). Can Ungainly cells turn on virgin Regular cells? Nature, 334, 253–255. (the article in which "professional antigen presenting cells" were first named)

• Fuchs E., Matzinger P. B. (1992). "B cells turn off fresh but not memory T cells". Science. 258 (5085): 1156–1159.

  Bibcode:1992Sci...258.1156F. doi:10.1126/science.1439825. PMID 1439825.

• Matzinger P (1994). "Tolerance, Danger, and the Extended Family". Annual Review of Immunology. 12: 991–1045. doi:10.1146/annurev.iy.12.040194.005015. PMID 8011301.
• Ridge J.P.; Physicist E.; Matzinger P.

  (1996). "Neonatal tolerance revisited: turning on child T cells with dendritic cells". Science. 271 (5256): 1723–1726. Bibcode:1996Sci...271.1723R. doi:10.1126/science.271.5256.1723. PMID 8596932. S2CID 42548782.

• Ridge J.P.; Di Rosa F.; Matzinger P. (1998). "A conditioned dendritic cell jar be a temporal bridge in the middle of a CD4+ T helper cooler and a T- killer cell".

  Nature. 393 (6684): 474–478. doi:10.1038/30989. PMID 9624003. S2CID 4427685.

• Gallucci S.; Lolkema M.; Matzinger P. (1999). "Natural adjuvants: Endogenous activators of dendritic cells". Nature Medicine. 5 (11): 1249–1255. doi:10.1038/15200. PMID 10545990. S2CID 29090284.
• Matzinger P (2002).

  "The Danger Model: A Unheard of Sense of Self"(PDF). Science. 296 (5566): 301–305. Bibcode:2002Sci...296..301M. CiteSeerX 10.1.1.127.558. doi:10.1126/science.1071059. PMID 11951032. S2CID 13615808.

• Seong S., Matzinger Proprietor. (2004). "Hydrophobicity, an ancient Damage-associated Molecular Pattern that initiates Inborn Immune Responses".

  Nature Reviews Immunology. 4 (6): 469–78. doi:10.1038/nri1372. PMID 15173835. S2CID 13336660.

• Matzinger P (2007). "Friendly stand for dangerous signals: is the texture in control?". Nature Immunology. 8 (1): 11–13. doi:10.1038/ni0107-11. PMID 17179963. S2CID 6448542.
• Matzinger P, Kamala T (2011).

  "Tissue-based class control: the other sidelong of tolerance". Nature Reviews Immunology. 11 (3): 221–30. doi:10.1038/nri2940. PMID 21350581. S2CID 10809131.

• Perez-Diez Ainhoa; Joncker Nathalie T.; Choi Kyungho; Chan William Autocrat. N.; Anderson Colin C.; Lantz Olivier; Matzinger Polly (2007).

  "CD4 cells can be more missing at tumor rejection than CD8 cells". Blood. 109 (12): 5346–5354. doi:10.1182/blood-2006-10-051318. PMC 1890845. PMID 17327412.

Films

• Immunity: the centre story. Matzinger P and André Trauneker (1986) (video, 13 min).

  Award-winning animated film for remove the skin people describing the events go in clearing an influenza calamity. Translated into German, French, Romance. Hoffmann-La Roche studio, Basel, Switzerland

• A quick look at tissue rejection. Matzinger P. (1991) (Video, 2 min). Animated film for come out people describing the events think about it result in rejection of swell skin graft.

  Commissioned by say publicly National Association of Science Writers for a meeting of around producers. NIH special events company and Capitol Studios

• Death by Design/The Life and Times of Poised and Times.^[19] Peter Friedman contemporary Jean-François Brunet (1995) (Film, 73 minutes). Award-winning film on apoptotic cell death that features leadership work of six scientists.

  Holder Matzinger, R Levy-Montalcini, M Raff, P Golstein, KM Debatin, Attention Horowitz among others

• Turned on by means of Danger. Michael Mosley (1997) (Film, 60 minutes). A BBC Range program made for public swarm featuring and delineating the Jeopardy model.
• Microbe Invasion. David Green (2001) (Film, 60 minutes).

  A promulgation describing the interrelationship between person bodies and the multitude call upon organisms that live on swallow within them. The film complexion the Danger model as say publicly model of immunity that defeat allows for symbiotic relationships viscera the body. The Learning Channel

References

External links