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Clark L. Anderson

April 14, 2024

Clark Lawrence Anderson is an internist and immunologist. He is professor emeritus in the Division of Immunology and Rheumatology, Department of Internal Medicine, Ohio State University (OSU), Columbus, Ohio, United States.

Education and personal life edit

Anderson studied medicine and biochemistry at the University of Chicago (MD 1964) after a grounding in the liberal arts at Brown University and the University of Arizona.[1] Upon being drafted as a physician into the Army during the Vietnam War, he served three years in Germany and then continued postgraduate education in internal medicine at the University of Colorado. Subsequent to postdoctoral research in immunochemistry with Richard Farr,[2] Percy Minden,[3] and Howard Grey[4] at the National Jewish Hospital in Denver, CO, he joined the faculty at the University of Rochester in 1977; and in 1986 he moved to OSU as professor in the Departments of Internal Medicine, Molecular and Cellular Biochemistry, and Molecular Genetics. Anderson is married to Carole Ann Anderson, administrator in higher education, former dean of the OSU College of Nursing, the College of Dentistry, and the Graduate School; former president of the American Association of Colleges of Nursing and fellow of the American Academy of Nursing.[5] The couple has three daughters.

Research areas edit

Anderson's academic career, funded continuously for more than 40 years by R01 grants from the National Institutes of Health, has focused on how Immunoglobulin G (IgG) antibodies mediate their cell biological effects through the family of Fcγ receptors (a class of Fc receptors that are members of the immunoglobulin superfamily).[6] His research contributions to biomedicine and immunology fall into four major groups:

1. The Fcγ Receptor (FcγR) family of molecules.[7][8] Anderson's early work on identifying and characterizing the high affinity FcγRI and low affinity FcγRII for IgG on human monocytes and other cells was aided by his development of monoclonal antibodies (mab) to both of these receptors, mab 32.2 (US Patent US4954617A awarded in 1990) to the former in collaboration with Michael Fanger and Paul Guyre,[9] and mab IV.3 to the latter in collaboration with R. John Looney.[10][11][12] To facilitate the clinical application of these antibodies, Anderson enabled the establishment by Fanger and Guyre of Medarex, Inc., a biotech company since acquired by Bristol-Myers Squibb for 2.4 billion $US.[13] Further studies by Anderson showed FcRI to be associated with the FcRγ chain, and that both receptors upon clustering mediated intracellular kinase cascades that triggered various biological effects. This early work catalyzed an avalanche of studies that have allowed the elaboration of the FcγR family of proteins, now known to consist of several genes (8 in human, 5 in mouse), over 20 transcripts, and at least 9 expressed protein receptors; further, it has become clear that clustering of these receptors results in a variety of biological effects such as superoxide and cytokine output, cell-mediated killing, endocytosis, all resulting in removal of the antigen and perversely in disease-causing auto-immune effects.[14]

2. IgG turnover mediated by the neonatal Fc receptor (FcRn)[15][16][17][18] Anderson, reading the published work of others describing IgG deficiency in the beta2-microglobulin knock out mouse,[19][20][21] realized that this strain was likely IgG deficient not because of low IgG production but because of rapid IgG degradation due to an FcRn deficiency. He formally affirmed this explanation by measuring the serum IgG decay rate in this KO strain.[22] Brambell's prediction of the 1960s was thus confirmed, that a single Fc receptor served both to transport IgG across the placenta and to divert IgG from degradation.[23] This high affinity characteristic of IgG for FcRn is exploited by the drug industry to prolong the lifespan of protein drugs.[24]

3. Albumin homeostasis mediated by FcRn. Anderson observed in vitro in detergent solution that albumin co-purified with a soluble variant of FcRn in roughly equimolar proportions, and realized that FcRn likely prolongs the half-life of albumin as it does IgG, thus explaining the lengthy lifespan of albumin in humans and lab animals. He formally affirmed this conclusion analyzing albumin decay in b2m and FcRn KO mouse strains,[25] and then showed that the two ligands bound to FcRn at different sites, independently, that the stoichiometric ratio of the IgG:FcRn:albumin interaction was 2:1:1, that comparison of the published sequences of FcRn in many species suggested that albumin bound to FcRn near the A peptide pocket, that the site on albumin responsible for interaction was the III domain.[26] Co-crystal studies by others have confirmed these conclusions.[27] Kinetic studies indicate that the evolution of FcRn was a great boon to metabolic economy: Were it not for the presence of FcRn the mouse would require a liver twice as large and an immune system five times larger to maintain albumin and IgG concentrations[28] The albumin-FcRn interaction described by Anderson has also been exploited by the pharmaceutical industry to prolong the lifespan of protein drugs.[24]

4. The removal of small particles from blood by liver sinusoidal endothelium (LSEC)[29] Anderson serendipitously observed that an astonishingly high fraction of the body's FcγRIIb was expressed in the sinusoidal endothelium of the liver. This receptor earlier had been studied only as an inhibitory molecule of the immune system. Rigorously exploring this observation, his laboratory found that fully 70% of the total body content of FcγRIIb is expressed in the sinusoidal endothelium; that FcγRIIb is unassociated with the FcRγ chain and thus likely does not convey inhibitory signals; that it mediates the uptake and ultimate degradation of small pinocytosable immune complexes.[30][31] His lab demonstrated in mice that HIV particles, in the absence of antibody opsonization, are taken up from blood and degraded by the liver sinusoidal endothelium at a rate of 100 million per minute.[32] These cells (LSEC) take up other viruses and other particles[33] in their capacity as the body's garbage dump, clearing small particles from the blood stream.

The distinctive features of Anderson's career have been the linearity of his scientific pursuit; the aggressive borrowing of technical solutions; a pursuit of basic and not translational questions; the publication of only model-changing work; collaborations only with helpers; a focus on hypothesis-denying experiments; an avoidance of review- and chapter-writing; no commercial backing but 40 years of continuous NIH R01 support.

Honors edit

  • Leukemia Society of America Special Fellow 1975-77
  • Research Career Development Award, NIAID 1979-84
  • Medical Biochemistry Study Section, DRG, NIH 1987-91
  • University Distinguished Scholar Award, OSU 1994

References edit

  1. ^ Clark Anderson Internal Medicine OSU
  2. ^ Farr RS (1958) A Quantitative Immunochemical Measure of the Primary Interaction Between I*BSA and Antibody. The Journal of Infectious Diseases, Volume 103, Issue 3, 1 November 1958, Pages 239–262, https://doi.org/10.1093/infdis/103.3.239
  3. ^ Farr R. and Minden P. (1968) Biology of the mycobacterioses. Ann N Y Acad Sci. 1968 Sep 5;154(1):107-14. PMID 4909582
  4. ^ National Academy of Sciences member page for Howard M. Grey
  5. ^ . hsl.osu.edu. Archived from the original on 2013-06-25.
  6. ^ Ohio State University, College of Medicine News article on $1.7M Grant awarded to Anderson in 2014
  7. ^ Anderson CL, Looney RJ. 1986. Human leukocyte IgG Fc receptors. Immunol Today. 1986 Sep;7(9):264-6. doi: 10.1016/0167-5699(86)90007-1. PMID 25290629
  8. ^ Anderson CL. 1989. Human IgG Fc receptors. Clin. Immunol. Immunopathol. 1989 Nov;53(2 Pt 2):S63-71. Review. PMID 2529071
  9. ^ Anderson CL, Guyre PM, Whitin JC, Ryan DH, Looney RJ, Fanger MW. (1986) Monoclonal antibodies to Fc receptors for IgG on human mononuclear phagocytes. Antibody characterization and induction of superoxide production in a monocyte cell line. J Biol Chem. Sep 25;261(27):12856-64
  10. ^ "The Celdara Team".
  11. ^ "The Celdara Team".
  12. ^ "Looney Lab - Rochester, NY - University of Rochester Medical Center".
  13. ^ Allison M. Bristol-Myers Squibb swallows last of antibody pioneers. Nat Biotechnol. 2009 Sep;27(9):781-3. doi: 10.1038/nbt0909-781. PMID 19741612
  14. ^ Nimmerjahn, F., and J. V. Ravetch. 2008. Fc receptors as regulators of immune responses. Nature Reviews Immunology 8: 34-47
  15. ^ Junghans RP, and Anderson CL. 1996. The protection receptor for IgG catabolism is the b2- microglobulin-containing neonatal intestinal transport receptor. Proc. Natl. Acad. Sci. 93:5512-5516.
  16. ^ Brambell FW (1969) The transmission of immune globulins from the mother to the foetal and newborn young. Proc Nutr Soc. 1969 Mar;28(1):35-41.
  17. ^ Ward ES, Ober RJ (2015) Commentary: “There’s been a flaw in our thinking”. Front. Immunol., 16 July 2015 | https://doi.org/10.3389/fimmu.2015.00351
  18. ^ Anderson CL (2014) Commentary: “There’s been a flaw in our thinking”. Front Immunol. 2014 Oct 31;5:540. doi: 10.3389/fimmu.2014.00540. eCollection 2014
  19. ^ Spriggs, M. K., B. H. Koller, T. Sato, P. J. Morrissey, W. C. Fanslow, O. Smithies, R. F. Voice, M. B. Widmer, and C. R. Maliszewski. 1992. Beta 2-microglobulin-, CD8+ T-cell-deficient mice survive inoculation with high doses of vaccinia virus and exhibit altered IgG responses. Proc. Natl. Acad. Sci. U. S. A. 89: 6070-6074.
  20. ^ Israel, E. J., V. K. Patel, S. F. Taylor, A. Marshak-Rothstein, and N. E. Simister. 1995. Requirement for a b2-microglobulin-associated Fc receptor for acquisition of maternal IgG by fetal and neonatal mice. J. Immunol. 154: 6246-6251.
  21. ^ Christianson, G. J., R. L. Blankenburg, T. M. Duffy, D. Panka, A. Marshak-Rothstein, J. B. Roths, and D. C. Roopenian. 1996. beta2-Microglobulin dependence of the lupus-like autoimmune syndrome of MRL-lpr mice. J. Immunol. 156: 4932-4939.
  22. ^ Junghans, R. P., and C. L. Anderson. 1996. The protection receptor for IgG catabolism is the b2-microglobulin-containing neonatal intestinal transport receptor. Proc. Natl. Acad. Sci. U. S. A. 93: 5512-5516.
  23. ^ Brambell, F. W. R. 1970. The Transmission of Passive Immunity from Mother to Young. North Holland Publishing Company, Amsterdam.
  24. ^ a b Sockolosky, J. T., and R. C. Szoka. 2017. The neonatal Fc receptor, FcRn, as a target for drug delivery and therapy. Adv drug Deliv Rev 91: 109-124.
  25. ^ Chaudhury, C., S. Mehnaz, J. M. Robinson, W. L. Hayton, D. K. Pearl, D. C. Roopenian, and C. L. Anderson. 2003. The major histocompatibility complex-related Fc receptor for IgG (FcRn) binds albumin and prolongs its lifespan. J. Exp. Med. 197: 315-322.
  26. ^ Chaudhury, C. 2005. Identification and biochemical characterization of a novel receptor: ligand interaction between FcRn and albumin. The Ohio State University. 1-95.
  27. ^ Schmidt, M. M., S. A. Townson, A. J. Andreucci, B. M. King, E. B. Schirmer, A. J. Murillo, C. Dombrowski, A. W. Tisdale, P. A. Lowden, A. L. Masci, J. T. Kovalchin, D. V. Erbe, K. D. Wittrup, E. S. Furfine, and T. M. Barnes. 2013. Crystal Structure of an HSA/FcRn Complex Reveals Recycling by Competitive Mimicry of HSA Ligands at a pH-Dependent Hydrophobic Interface. Structure.
  28. ^ Kim, J., C. L. Bronson, W. L. Hayton, M. D. Radmacher, D. C. Roopenian, J. M. Robinson, and C. L. Anderson. 2006. Albumin turnover: FcRn-mediated recycling saves as much albumin from degradation as the liver produces. Am J Physiol Gastrointest Liver Physiol 290: G352-G360.
  29. ^ Anderson, C. L. 2015. The liver sinusoidal endothelium reappears after being eclipsed by the Kupffer cell: a 20th century biological delusion corrected. J. Leukoc. Biol. 98: 875-876.
  30. ^ Ganesan, L. P., S. Mohanty, J. Kim, K. R. Clark, J. M. Robinson, and C. L. Anderson. 2011. Rapid and Efficient Clearance of Blood-borne Virus by Liver Sinusoidal Endothelium 1. PLoS. Pathog. 7: e1002281
  31. ^ Ganesan, L. P., J. Kim, Y. Wu, S. Mohanty, G. S. Phillips, D. J. Birmingham, J. M. Robinson, and C. L. Anderson. 2012. FcgammaRIIb on Liver Sinusoidal Endothelium Clears Small Immune Complexes. J. Immunol. 189: 4981-4988.
  32. ^ Mates, J. M., Z. Yao, A. M. Cheplowitz, O. Suer, G. S. Phillips, J. J. Kwiek, M. V. Rajaram, J. Kim, J. M. Robinson, L. P. Ganesan, and C. L. Anderson. 2017. Mouse Liver Sinusoidal Endothelium Eliminates HIV-Like Particles from Blood at a Rate of 100 Million per Minute by a Second-Order Kinetic Process. Front Immunol. 8: 35.
  33. ^ Yao, Z., J. M. Mates, A. M. Cheplowitz, L. P. Hammer, A. Maiseyeu, G. S. Phillips, M. D. Wewers, M. V. Rajaram, J. M. Robinson, C. L. Anderson, and L. P. Ganesan. 2016. Blood-Borne Lipopolysaccharide Is Rapidly Eliminated by Liver Sinusoidal Endothelial Cells via High-Density Lipoprotein. J. Immunol. 197: 2390-2399.

External links edit

  • Anderson Lab

April 14, 2024
clark, anderson, clark, lawrence, anderson, internist, immunologist, professor, emeritus, division, immunology, rheumatology, department, internal, medicine, ohio, state, university, columbus, ohio, united, states, contents, education, personal, life, research. Clark Lawrence Anderson is an internist and immunologist He is professor emeritus in the Division of Immunology and Rheumatology Department of Internal Medicine Ohio State University OSU Columbus Ohio United States Contents 1 Education and personal life 2 Research areas 3 Honors 4 References 5 External linksEducation and personal life editAnderson studied medicine and biochemistry at the University of Chicago MD 1964 after a grounding in the liberal arts at Brown University and the University of Arizona 1 Upon being drafted as a physician into the Army during the Vietnam War he served three years in Germany and then continued postgraduate education in internal medicine at the University of Colorado Subsequent to postdoctoral research in immunochemistry with Richard Farr 2 Percy Minden 3 and Howard Grey 4 at the National Jewish Hospital in Denver CO he joined the faculty at the University of Rochester in 1977 and in 1986 he moved to OSU as professor in the Departments of Internal Medicine Molecular and Cellular Biochemistry and Molecular Genetics Anderson is married to Carole Ann Anderson administrator in higher education former dean of the OSU College of Nursing the College of Dentistry and the Graduate School former president of the American Association of Colleges of Nursing and fellow of the American Academy of Nursing 5 The couple has three daughters Research areas editAnderson s academic career funded continuously for more than 40 years by R01 grants from the National Institutes of Health has focused on how Immunoglobulin G IgG antibodies mediate their cell biological effects through the family of Fcg receptors a class of Fc receptors that are members of the immunoglobulin superfamily 6 His research contributions to biomedicine and immunology fall into four major groups 1 The Fcg Receptor FcgR family of molecules 7 8 Anderson s early work on identifying and characterizing the high affinity FcgRI and low affinity FcgRII for IgG on human monocytes and other cells was aided by his development of monoclonal antibodies mab to both of these receptors mab 32 2 US Patent US4954617A awarded in 1990 to the former in collaboration with Michael Fanger and Paul Guyre 9 and mab IV 3 to the latter in collaboration with R John Looney 10 11 12 To facilitate the clinical application of these antibodies Anderson enabled the establishment by Fanger and Guyre of Medarex Inc a biotech company since acquired by Bristol Myers Squibb for 2 4 billion US 13 Further studies by Anderson showed FcRI to be associated with the FcRg chain and that both receptors upon clustering mediated intracellular kinase cascades that triggered various biological effects This early work catalyzed an avalanche of studies that have allowed the elaboration of the FcgR family of proteins now known to consist of several genes 8 in human 5 in mouse over 20 transcripts and at least 9 expressed protein receptors further it has become clear that clustering of these receptors results in a variety of biological effects such as superoxide and cytokine output cell mediated killing endocytosis all resulting in removal of the antigen and perversely in disease causing auto immune effects 14 2 IgG turnover mediated by the neonatal Fc receptor FcRn 15 16 17 18 Anderson reading the published work of others describing IgG deficiency in the beta2 microglobulin knock out mouse 19 20 21 realized that this strain was likely IgG deficient not because of low IgG production but because of rapid IgG degradation due to an FcRn deficiency He formally affirmed this explanation by measuring the serum IgG decay rate in this KO strain 22 Brambell s prediction of the 1960s was thus confirmed that a single Fc receptor served both to transport IgG across the placenta and to divert IgG from degradation 23 This high affinity characteristic of IgG for FcRn is exploited by the drug industry to prolong the lifespan of protein drugs 24 3 Albumin homeostasis mediated by FcRn Anderson observed in vitro in detergent solution that albumin co purified with a soluble variant of FcRn in roughly equimolar proportions and realized that FcRn likely prolongs the half life of albumin as it does IgG thus explaining the lengthy lifespan of albumin in humans and lab animals He formally affirmed this conclusion analyzing albumin decay in b2m and FcRn KO mouse strains 25 and then showed that the two ligands bound to FcRn at different sites independently that the stoichiometric ratio of the IgG FcRn albumin interaction was 2 1 1 that comparison of the published sequences of FcRn in many species suggested that albumin bound to FcRn near the A peptide pocket that the site on albumin responsible for interaction was the III domain 26 Co crystal studies by others have confirmed these conclusions 27 Kinetic studies indicate that the evolution of FcRn was a great boon to metabolic economy Were it not for the presence of FcRn the mouse would require a liver twice as large and an immune system five times larger to maintain albumin and IgG concentrations 28 The albumin FcRn interaction described by Anderson has also been exploited by the pharmaceutical industry to prolong the lifespan of protein drugs 24 4 The removal of small particles from blood by liver sinusoidal endothelium LSEC 29 Anderson serendipitously observed that an astonishingly high fraction of the body s FcgRIIb was expressed in the sinusoidal endothelium of the liver This receptor earlier had been studied only as an inhibitory molecule of the immune system Rigorously exploring this observation his laboratory found that fully 70 of the total body content of FcgRIIb is expressed in the sinusoidal endothelium that FcgRIIb is unassociated with the FcRg chain and thus likely does not convey inhibitory signals that it mediates the uptake and ultimate degradation of small pinocytosable immune complexes 30 31 His lab demonstrated in mice that HIV particles in the absence of antibody opsonization are taken up from blood and degraded by the liver sinusoidal endothelium at a rate of 100 million per minute 32 These cells LSEC take up other viruses and other particles 33 in their capacity as the body s garbage dump clearing small particles from the blood stream The distinctive features of Anderson s career have been the linearity of his scientific pursuit the aggressive borrowing of technical solutions a pursuit of basic and not translational questions the publication of only model changing work collaborations only with helpers a focus on hypothesis denying experiments an avoidance of review and chapter writing no commercial backing but 40 years of continuous NIH R01 support Honors editLeukemia Society of America Special Fellow 1975 77 Research Career Development Award NIAID 1979 84 Medical Biochemistry Study Section DRG NIH 1987 91 University Distinguished Scholar Award OSU 1994References edit Clark Anderson Internal Medicine OSU Farr RS 1958 A Quantitative Immunochemical Measure of the Primary Interaction Between I BSA and Antibody The Journal of Infectious Diseases Volume 103 Issue 3 1 November 1958 Pages 239 262 https doi org 10 1093 infdis 103 3 239 Farr R and Minden P 1968 Biology of the mycobacterioses Ann N Y Acad Sci 1968 Sep 5 154 1 107 14 PMID 4909582 National Academy of Sciences member page for Howard M Grey Carole A Anderson Health Sciences Library hsl osu edu Archived from the original on 2013 06 25 Ohio State University College of Medicine News article on 1 7M Grant awarded to Anderson in 2014 Anderson CL Looney RJ 1986 Human leukocyte IgG Fc receptors Immunol Today 1986 Sep 7 9 264 6 doi 10 1016 0167 5699 86 90007 1 PMID 25290629 Anderson CL 1989 Human IgG Fc receptors Clin Immunol Immunopathol 1989 Nov 53 2 Pt 2 S63 71 Review PMID 2529071 Anderson CL Guyre PM Whitin JC Ryan DH Looney RJ Fanger MW 1986 Monoclonal antibodies to Fc receptors for IgG on human mononuclear phagocytes Antibody characterization and induction of superoxide production in a monocyte cell line J Biol Chem Sep 25 261 27 12856 64 The Celdara Team The Celdara Team Looney Lab Rochester NY University of Rochester Medical Center Allison M Bristol Myers Squibb swallows last of antibody pioneers Nat Biotechnol 2009 Sep 27 9 781 3 doi 10 1038 nbt0909 781 PMID 19741612 Nimmerjahn F and J V Ravetch 2008 Fc receptors as regulators of immune responses Nature Reviews Immunology 8 34 47 Junghans RP and Anderson CL 1996 The protection receptor for IgG catabolism is the b2 microglobulin containing neonatal intestinal transport receptor Proc Natl Acad Sci 93 5512 5516 Brambell FW 1969 The transmission of immune globulins from the mother to the foetal and newborn young Proc Nutr Soc 1969 Mar 28 1 35 41 Ward ES Ober RJ 2015 Commentary There s been a flaw in our thinking Front Immunol 16 July 2015 https doi org 10 3389 fimmu 2015 00351 Anderson CL 2014 Commentary There s been a flaw in our thinking Front Immunol 2014 Oct 31 5 540 doi 10 3389 fimmu 2014 00540 eCollection 2014 Spriggs M K B H Koller T Sato P J Morrissey W C Fanslow O Smithies R F Voice M B Widmer and C R Maliszewski 1992 Beta 2 microglobulin CD8 T cell deficient mice survive inoculation with high doses of vaccinia virus and exhibit altered IgG responses Proc Natl Acad Sci U S A 89 6070 6074 Israel E J V K Patel S F Taylor A Marshak Rothstein and N E Simister 1995 Requirement for a b2 microglobulin associated Fc receptor for acquisition of maternal IgG by fetal and neonatal mice J Immunol 154 6246 6251 Christianson G J R L Blankenburg T M Duffy D Panka A Marshak Rothstein J B Roths and D C Roopenian 1996 beta2 Microglobulin dependence of the lupus like autoimmune syndrome of MRL lpr mice J Immunol 156 4932 4939 Junghans R P and C L Anderson 1996 The protection receptor for IgG catabolism is the b2 microglobulin containing neonatal intestinal transport receptor Proc Natl Acad Sci U S A 93 5512 5516 Brambell F W R 1970 The Transmission of Passive Immunity from Mother to Young North Holland Publishing Company Amsterdam a b Sockolosky J T and R C Szoka 2017 The neonatal Fc receptor FcRn as a target for drug delivery and therapy Adv drug Deliv Rev 91 109 124 Chaudhury C S Mehnaz J M Robinson W L Hayton D K Pearl D C Roopenian and C L Anderson 2003 The major histocompatibility complex related Fc receptor for IgG FcRn binds albumin and prolongs its lifespan J Exp Med 197 315 322 Chaudhury C 2005 Identification and biochemical characterization of a novel receptor ligand interaction between FcRn and albumin The Ohio State University 1 95 Schmidt M M S A Townson A J Andreucci B M King E B Schirmer A J Murillo C Dombrowski A W Tisdale P A Lowden A L Masci J T Kovalchin D V Erbe K D Wittrup E S Furfine and T M Barnes 2013 Crystal Structure of an HSA FcRn Complex Reveals Recycling by Competitive Mimicry of HSA Ligands at a pH Dependent Hydrophobic Interface Structure Kim J C L Bronson W L Hayton M D Radmacher D C Roopenian J M Robinson and C L Anderson 2006 Albumin turnover FcRn mediated recycling saves as much albumin from degradation as the liver produces Am J Physiol Gastrointest Liver Physiol 290 G352 G360 Anderson C L 2015 The liver sinusoidal endothelium reappears after being eclipsed by the Kupffer cell a 20th century biological delusion corrected J Leukoc Biol 98 875 876 Ganesan L P S Mohanty J Kim K R Clark J M Robinson and C L Anderson 2011 Rapid and Efficient Clearance of Blood borne Virus by Liver Sinusoidal Endothelium 1 PLoS Pathog 7 e1002281 Ganesan L P J Kim Y Wu S Mohanty G S Phillips D J Birmingham J M Robinson and C L Anderson 2012 FcgammaRIIb on Liver Sinusoidal Endothelium Clears Small Immune Complexes J Immunol 189 4981 4988 Mates J M Z Yao A M Cheplowitz O Suer G S Phillips J J Kwiek M V Rajaram J Kim J M Robinson L P Ganesan and C L Anderson 2017 Mouse Liver Sinusoidal Endothelium Eliminates HIV Like Particles from Blood at a Rate of 100 Million per Minute by a Second Order Kinetic Process Front Immunol 8 35 Yao Z J M Mates A M Cheplowitz L P Hammer A Maiseyeu G S Phillips M D Wewers M V Rajaram J M Robinson C L Anderson and L P Ganesan 2016 Blood Borne Lipopolysaccharide Is Rapidly Eliminated by Liver Sinusoidal Endothelial Cells via High Density Lipoprotein J Immunol 197 2390 2399 External links editAnderson Lab Retrieved from https en wikipedia org w index php title Clark L Anderson amp oldid 1216013902, wikipedia, wiki, book, books, library,

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