Investigator and Head, Center for Immunology and Inflammation
The Feinstein Institute for Medical Research
350 Community Drive, 4th Floor

Tel:  516-562-3402
Fax: 516-562-1022
Email: bsherry@nshs.edu

Education:
BA, 1975,  Smith College
PhD, 1986,  Brandeis University

Appointments:
Associate Professor, Department of Medicine, NYU School of Medicine
Associate Professor, Elmezzi Graduate School of Molecular Medicine

Dr. Barbara Sherry’s laboratory investigates the biology of chemokines and their receptors. Chemokines are a class of secreted proteins that regulate cell movement and serve as the “traffic cops” of the immune system.  They play a critical role in host defense and immune system homeostasis. Studies in Dr. Sherry’s laboratory are focused on elucidating the biological role of these molecules in the host response to bacterial and viral infections and neoplastic disease. Ultimately, these studies will reveal mechanisms for controlling innate immune responses during infection to improve clinical outcomes.
 
Dr. Sherry’s research team has recently discovered that chemokine-mediated cell trafficking is globally impaired in patients who suffer from systemic infections and sepsis. This defective trafficking may contribute to the increased susceptibility to secondary infections, impaired wound healing and poor survival observed in these patients. Dr. Sherry’s laboratory is working to define the molecular mechanisms that trigger this impairment. These studies will lead to the identification of new targets for immune regulation and therapeutic intervention in this high-risk group. Dr. Sherry’s laboratory is also exploring whether defective cell trafficking in response to chemokines contributes to other clinical syndromes that are associated with increased susceptibility to infection, including end-stage renal disease.
 
Dr. Sherry and her colleagues are also studying how the body’s immune system responds to HIV infection. One of the reasons that AIDS is such a devastating disease is that the virus is able to evade or subvert many of those natural defense mechanisms and Dr. Sherry’s laboratory is trying to understand how the virus is able to do this so effectively. They have recently identified a previously unrecognized mechanism by which HIV type 1 (HIV 1) subverts host chemokine responses - a discovery that opens the door to the development of new therapeutic strategies to improve immune function in HIV 1-infected individuals. They are now collaborating with physicians at North Shore University Hospital’s division of Infectious Disease to determine if a similar phenomenon occurs in people infected with HIV.
 

Research Activities of the Laboratory of Cytokine Biology 

The innate immune system is the first line of defense against invasive trespassers, including bacteria, viruses, parasites, and tumors.  Our laboratory has had a long-standing interest in the mechanisms that coordinate the innate immune response.  Early work led to the discovery of a novel set of heparin-binding chemoattractant molecules produced by cells in response to bacterial challenge, and the identification that those proteins were in fact members of a larger family of proteins, the chemokine family, whose actions are critical for both host defense and immune system homeostasis.  As with other inflammatory cytokines, though, we now recognize that excessive production of these same chemokine proteins and/or dysregulation of chemokine receptor expression can be detrimental, contributing to disease-associated pathology. Our ongoing research goal is to gain a better understanding of the molecular mechanisms that regulate chemokine and chemokine receptor responses.   Our efforts are concentrated in the following areas:

Chemokine Receptor Regulation in Inflammation, Infection, and Sepsis

In the context of bacterial infection, our studies focus on aberrant chemokine and chemokine receptor expression that contribute to tissue and organ damage early in infection, and host immunosuppression late in infection.  One of the principal complications of sepsis syndrome, a potentially lethal illness triggered by systemic bacterial infection, is increased susceptibility to secondary lung infections.  Macrophages are known to play an essential role in the resolution phase of pulmonary infection, and they are recruited to the lung by chemokine/chemokine receptor interactions.  Our studies have shown that exposure of macrophages to LPS, a major constituent of gram-negative bacteria, downregulates two chemokine receptors (CCR1 and CCR5), thereby markedly impairing the ability of affected cells to migrate in response to chemokine signals.  We are currently using dominant negative mutant, siRNA, and pharmacologic inhibitor strategies to elucidate the mechanisms that contribute to LPS-triggered downregulation of chemokine receptors in macrophages, and to establish a link between chemokine receptor downregulation and increased susceptibility to secondary infection.  We are also exploring the hypothesis that chemokine receptor impairment, which leaves leukocytes unresponsive to migratory signals critical for host defense, places septic patients at increased risk for developing secondary infections.  We have recently begun an NIH funded collaborative study with Drs. Dana Lustbader, Marcia Epstein, and Erfan Hussain to assess whether chemokine receptor expression is suppressed in circulating leukocytes isolated from septic patients, and if so, to evaluate whether this defect correlates with increased susceptibility to secondary lung infection.  The results gained from this study will improve our understanding of chemokine/chemokine receptor interactions within the context of sepsis, provide valuable insight into why inflammatory responses are impaired in septic patients, and encourage the development of new therapeutic strategies to prevent and to control secondary lung infections in sepsis.

Mechanisms contributing to impaired innate immune responses in end stage renal disease

Patients with end stage renal disease (ESRD), especially those on dialysis, are at increased risk for serious bacterial infections.  The early inflammatory response is decreased in dialysis patients and abnormalities in macrophage and neutrophil function contribute to their increased susceptibility to infection.  The cellular and molecular basis for the immune dysfunction observed in patients with ESRD is not fully understood.  Chemokine receptors are critical regulators of macrophage and neutrophil trafficking and activation state, and we are currently studying whether chemokine receptor expression and/or function is dysregulated in patients with ESRD, contributing to leukocyte dysfunction.  In collaborative studies with Dr. Howard Trachtman at Schneider Children’s Hospital, we have shown that ESRD is associated with reduced expression of the chemokine receptors CXCR1 and CCR2 on circulating neutrophils and monocytes, respectively.  Chemokine receptor impairment is most dramatic in a subpopulation of patients that have had three or more infections in the preceding twelve months.  We have further shown that reduced chemokine receptor expression on peripheral blood leukocytes results in failure of these cells to respond to chemokine-mediated trafficking signals.  These data provide a better understanding of the immune dysfunction involved in the pathogenesis of catheter-related infections in children with ESRD on dialysis, and may help identify a subset of patients at increased risk of developing serious bacterial infections.  We are now carrying out studies to determine the mechanisms that contribute to chemokine receptor dysregulation in ESRD.

Regulation of host antiviral β-chemokine responses in HIV-infected individuals

Paradoxically, chemokine receptors, critical for the transduction of intracellular signals that promote innate immune responses, are sometimes used by intracellular pathogens to facilitate their entry into cells and/or their transmission.  Seminal studies by others revealed that a subset of chemokine receptors function as co-receptors for HIV 1, and that chemokines (the natural ligands for one of the HIV-1 co-receptor CCR5) exert potent anti-viral effects in T cells, presumably through their ability to interfere with viral co-receptor usage.  Several recent reports indicate that chemokine responses are defective in HIV-infected individuals, although the molecular basis for this defect is not fully understood.  Our focus is on identifying mechanisms whereby HIV-1 manipulates host anti-viral β-chemokine responses to its own benefit and assessing whether dysregulated chemokine responses may underlie abnormal cellular trafficking in patients with AIDS. We have recently identified a previously unrecognized mechanism by which HIV type 1 (HIV-1) subverts the innate immune response- a discovery that opens the door to the development of new therapeutic strategies to improve immune function in HIV-1-infected individuals.  On another front, we are identifying potential mechanisms that negatively regulate β-chemokine receptor (CCR5) expression and inhibit HIV-1 infection.  In differentiated macrophages, an important cellular reservoir for the virus in vivo, we have shown that LPS activation markedly downregulates CCR5 receptor expression making these cells effectively resistant to HIV-1 infection.  This LPS-mediated down-regulation is independent of de novo protein synthesis and differs from the rapid turnover of CCR5 in response to its natural ligands. Our current work focuses on defining the underlying mechanisms (transcriptional blockade, post-translational modification, altered recycling, enhanced degradation), which lead to sustained downregulation of β-chemokine receptors in macrophages exposed to LPS, and characterizing the ramifications of this process for macrophage susceptibility to HIV infection.

Role of Chemokines in B Cell Chronic Lymphocytic Leukemia

B Cell Chronic Lymphocytic Leukemia (B-CLL) is a B-cell malignancy that is characterized by the accumulation of monoclonal CD5+ B cells in the blood and tissues.  Signals provided by the microenvironment are known to greatly influence the growth and survival of CLL cells.  Some of these conditioning signals are provided by chemokines, a family of chemotactic proteins that play a role in both host defense and immune system homeostasis   We are currently collaborating with Dr. Nicholas Chiorazzi and members of the CLL Research and Treatment Program at The Feinstein to better understand the role of chemokine mediated trafficking and survival signals in the growth and survival of CLL cells, and the factors that regulate the expression of chemokines within the leukemic microenvironment.

Ovarian Cancer Discovery Program

We are currently developing a collaborative discovery program to identify potential risk factors and early diagnostic markers for ovarian cancer.  In conjunction with the Tissue Donation Program, we are collaborating with Christine Metz, PhD, Peter Gregersen, MD, John Lovecchio, MD, and the members of the Department of Gynecology Oncology to collect important biological samples for this program.

---

Lab Members:

Name:    Mohammad Javdan, PhD
Title:    Research Scientist
Education: BS in Biology, 1986, University of Tehran
MS in Anatomy, 1990, Tehran University of Medical Sciences
PhD, 1995, Tehran University of Medical Sciences
Research: Regulation of leukocyte trafficking and adhesion in acute and chronic infection; Chemokine receptor regulation in sepsis.
E-mail:    mjavdan@nshs.edu

Name:    Paulina (Pui Yan) Chiu, MS/MBA
Title:    Research Associate
Education: B.S. in Biology, 1990, King College
MS in Nutrition, 1993, The Pennsylvania State University
MBA in Health Services Management, 2008, Hofstra University
Research: Elucidation of the molecular mechanisms regulating LPS-triggered chemokine receptor downregulation in macrophages; Characterization of chemokine responses in patients with sepsis, end stage renal disease, and HIV infection.
E-mail:    pchiu@nshs.edu

Name: Preetesh Jain, MBBS,MD,ECMO,DM
Position: Post Doc Research Fellow, CLL Research and Treatment Program
Education: MBBS, 1999, Vijaynagar Institute of Medical Science, India; MD, 2003, Rabindra Nath Tagore (RNT) Medical College, India
Research: Characterization of the role of chemokines, their receptors and Th17 cells in B cell chronic lymphocytic leukemia (B-CLL)
E-mail:     mjavdan@nshs.edu

Name:   Beatrice Goilav, MD
Position: Attending, Pediatric Nephrology, Schneider Children's Hospital
Assistant Professor of Pediatrics, Albert Einstein College of Medicine, Yeshiva University
Education: MD, 1999, Basal University, Switzerland
Research: Characterization of the effect of different stages of chronic kidney disease on the innate immune system, specifically toll-like receptor signaling and chemokine receptor expression and function.
E-mail: bgoilav@nshs.edu

---

Collaborators:

Christine Metz, PhD
Nicholas Chiorazzi, MD
Howard Trachtman, MD
Dana Lustbader, MD
Marcia Epstein, MD
Erfan Hussain, MD
Yousef Al-Abed, MD
Edmund Miller, PhD
Marc Symons, PhD
John Lovecchio, MD
Peter K Gregersen, MD
Percio Gulko, MD
Kevin J Tracey, MD

Selected Publications:

Sherry B, Dai WW, Lesser ML, Trachtman H (2008) Dysregulated chemokine receptor expression and chemokine-mediated cell trafficking in pediatric patients with ESRD.  Clin J Am Soc Neph. 3:397-406.

Yurchenko V, Xue Z, Sherry B, Bukrinsky M (2008) Functional analysis of Leishmania major cyclophilin. Int J Parasitol. 38:633-9.

Wapnir RA, Sherry B, Codipilly CN, Goodwin LO, Vancurova I (2008) Modulation of Rat Intestinal Nuclear Factor NF-kappa B by Gum Arabic. Dig Dis Sci. 53:80-87.

Laragione T, Yarlett NC, Brenner M, Mello A, Sherry B, Miller EJ, Metz CN, Gulko PS (2007) The arthritis severity quantitative trait loci (QTL) Cia4 and Cia6 regulate neutrophil migration into inflammatory sites and levels of TNF beta and nitric oxide. J Immunol. 178:2344-2351.

Laragione T, Brenner M, Yarlett NC, Mello A, Miller EJ, Metz CN, Sherry B, Gulko PS (2007) The arthritis severity quantitative trait locus (QTL) Cia7 regulates neutrophil migration into inflammatory sites. Genes and Immunity 8:147-153.

Qin, S, Wang H, Yuan R, Li H, Ochani M, Ochani K, Rosas-Ballina M, Czura CJ, Huston JM, Miller E, Lin X, Sherry B, Kuman A, LaRosa G, Newman W, Tracey KJ Yang H (2006) Role of HMGB1 in apoptosis-mediated sepsis lethality. J Exp Med. 203:1637-1642.

Ghezzi P, Casagrande S, Massignan T, Basso M, Bellacchio E, Mollica L, Biasini E, Tonelli R, Eberini I, Gianazza E, Dai WW, Gratelli M, Salmona M, Sherry B, Bonetto V (2006) Redox regulation of cyclophilin A by glutathionylation. Proteomics 6:817-825.

Di Marzio P, Dai WW, Franchin G, Chan AY, Symons M, Sherry B (2005) Role of Rho family GTPases in CCR1- and CCR5-induced actin reorganization in macrophages. BBRC 331:909-916.

Pushkarsky T, Yurchenko V, Vanpouille C, Brichacek B, Vaisman I, Hatakeyama S, Nakayama KI, Sherry B, Bukrinsky MI (2005) Cell surface expression of CD147/EMMPRIN is regulated by cyclophilin 60.  J Biol Chem. 280:27866-27871.

Saeed RW, Varma S, Peng-Nemeroff T, Sherry B, Balakhaneh D, Huston J, Tracey KJ, Al-Abed Y, Metz CN (2005) Cholinergic stimulation blocks endothelial cell activation and leukocyte recruitment during inflammation. J Exp Med. 201:1113-1123.

Amella, CA, Sherry, B, Shepp, D, Schmidtmayerova, H (2005) Macrophage inflammatory protein 1 alpha  inhibits post-entry steps of HIV-1 infection via suppression of intracellular cAMP. J.Virol. 79:5625-5631.

Yurchenko V, Pushkarsky T, Li JH, Dai WW, Sherry B, Bukrinsky M (2005) Regulation of CD147 cell surface expression: involvement of the proline residue in the CD147 transmembrane domain. J Biol Chem. 280:17013-17019.

Saeed RW, Varma S, Peng T, Tracey KJ, Sherry B, Metz CN (2004) Ethanol blocks leukocyte recruitment and endothelial cell activation in vivo and in vitro. J Immunol. 173:6376-6383.

Gross E, Amella CA, Pompucci L, Franchin G, Sherry B, Schmidtmayerova H. (2003) Macrophages and lymphocytes differentially modulate the ability of RANTES to inhibit HIV 1 infection. J. Leuk. Biol. 74:781-790.

Di Marzio P, Sherry B, Thomas EK, Franchin G, Schmidtmayerova H, Bukrinsky M. (2003) Beta-Chemokine production in CD40L-stimulated monocyte-derived-macrophages requires activation of MAPK signaling pathway. Cytokine 23:53-63.

Oyajobi BO, Franchin G, Williams PJ, Pulkrabek D, Gupta A, Munoz S, Grubbs B, Zhao M, Chen D, Sherry B, Mundy GR. (2003) Dual effects of macrophage inflammatory protein 1alpha on osteolysis and tumor burden in the murine 5TGM1 model of myeloma bone disease. Blood 102:311-319.

Yurchenko V, Zybarth G, O'Connor M, Dai WW, Franchin G, Hao T, Guo H, Hung HC, Toole B, Gallay P, Sherry B, Bukrinsky M (2002) Active site residues of cyclophilin A are crucial for its signaling activity via CD147. J. Biol. Chem. 277:22959-22965.

Pushkarsky T, Zybarth G, Dubrovsky L, Yurchenko V, Tang H, Guo H, Toole B, Sherry B, Bukrinsky M  (2001) CD147 facilitates HIV 1 infection by interacting with virus associated cyclophilin A. Proc. Natl. Acad. Sci. U.S.A. 98:6360 6365.

Sherry B, Franchin G (2000) MIP-1α, MIP-1β.  In: Cytokine Reference: A compendium of cytokines and other mediators of host defense. Volume I. Oppenheim J.J. and Feldmann M. (eds.), Academic Press, San Diego, pp. 1171-1215.

Sherry B, Schmidtmayerova H, Zybarth G, Dubrovsky L, Raabe T, Bukrinsky M (2000) Nitric oxide regulates MIP-1α expression in primary macrophages and T lymphocytes: Implications for anti-HIV-1 response.  Molecular Medicine 6:542-549.

Franchin G, Zybarth G, Dai WW, Dubrovsk, I, Reiling N, Schmidtmayerova H, Bukrinsky M, Sherry B (2000) Lipopolysaccharide inhibits HIV-1 infection of monocyte-derived macrophages through direct and sustained down-regulation of CC chemokine receptor 5. J. Immunol. 164:2592-2601.

Martiney JA, Sherry B, Metz CN, Espinoza M, Ferrer AS, Calandra T, Broxmeyer HE, Bucala R (2000) Macrophage migration inhibitory factor release by macrophages after ingestion of Plasmodium chabaudi-infected erythrocytes: Possible role in the pathogenesis of malarial anemia.  Infect. Immun. 68:2259-2267.

Zybarth G, Reiling N, Schmidtmayerova H, Sherry B, Bukrinsky M (1999) Activation-induced resistance of human macrophages to HIV-1 infection in vitro.  J. Immunol. 162:400-406.

Sherry B, Espinoza M, Manogue KR Cerami A (1998) Induction of the chemokine β peptides, MIP-1α and MIP-1β, by lipopolysaccharide is differentially regulated by immunomodulatory cytokines γ IFN, IL-10, IL-4, and TGF-β.  Molecular Medicine 4:648-657.

Wang H, Zhang M, Bianchi M, Sherry B, Sama A, Tracey KJ (1998) Fetuin (α 2-HS-glycoprotein) opsonizes cationic macrophage deactivating molecules.  Proc. Natl. Acad. Sci. USA. 95:14429-14434.

Sherry B, Zybarth G, Alfano M, Dubrovsky L, Mitchell R, Rich D, Ulrich P, Bucala R, Cerami A, Bukrinsky M (1998) Role of cyclophilin A in the uptake of HIV-1 by macrophages and T lymphocytes. Proc. Natl. Acad. Sci. USA. 95:1758-1763.

Wu X, Dolecki GJ, Sherry B, Zagorski J, Lefkowith JB (1997) Chemokines are expressed in a myeloid cell-dependent fashion and mediate distinct functions in immune complex glomerulonephritis in rat.  J. Immunol. 158:3917-3924.

Zhang M, Caragine T, Wang H, Cohen PS, Botchkina G, Soda K, Bianchi M, Ulrich P, Cerami A, Sherry B, Tracey KJ (1997) Spermine inhibits pro-inflammatory cytokine synthesis in human mononuclear cells: A counter-regulatory mechanism that restrains the immune system. J. Exp. Med. 185:1759-1768.

Maric M, Chen L, Sherry B, Liu Y (1997) A mechanism for selective recruitment of CD8 T cells inot B7-1-transfected plasmacytoma: Role of macrophage inflammatory protein-1α.  J. Immunol. 159:360-368.

Schmidtmayerova H, Sherry B, Bukrinsky M (1996) Differential effect of β chemokines on HIV-1 replication in T lymphocytes and monocytes.   Nature 382:767.

Karp CL, Wysocka M, Wahl LM, Ahearn JM, Cuomo PJ, Sherry B, Trinchieri G, Griffin DE (1996) Mechanism of suppression of cell-mediated immunity by measles virus.  Science 273:228-231.

Schmidtmayerova H, Nottet HS, Nuovo LM, Raabe G, Flanagan T,  Dubrovsky CR, Gendelman L,  Cerami A, Bukrinsky M, Sherry B  (1996) HIV 1 infection alters chemokine β peptide expression in human monocytes: Implications for recruitment of leukocytes into brain and lymph nodes.  Proc. Natl. Acad. Sci. USA. 93:700-704.

Sherry B, Alava G, Tracey KJ, Martiney J, Cerami A, Slater AFG (1995) The malaria-specific metabolite hemozoin mediates the release of several potent endogenous pyrogens (TNF, MIP 1α, and MIP 1β) in vitro, and altered thermoregulation in vivo.  J. Inflammation. 45:85-86.

Sherry B, Cerami A (1993) Macrophage inflammatory protein-1 Cytokines of the Lung, Kelly, J. (ed.) Marcel Dekker, Inc., New York 61:369-380.

Widmer U, Manogue KR, Cerami A, Sherry B (1993) Genomic cloning and promoter analysis of macrophage inflammatory protein (MIP) 2, MIP 1α, and MIP 1β members of the chemokine superfamily of pro-inflammatory cytokines.  J. Immunol. 150:4996-5012.

Broxmeyer HE, Sherry B, Cooper S, Lu L, Maze R, Beckmann MP, Cerami A, Ralph P (1993) Comparative analysis of the human macrophage inflammatory protein family of cytokines (chemokines) on proliferation of human myeloid progenitor cells.  Interacting effects involving suppression, synergistic suppression, and blocking of suppression.  J. Immunol. 150:3448-3458.

Maze R, Sherry B, Kwon BS, Cerami A, Broxmeyer HE (1992) Myelosuppressive effects in vivo of purified recombinant murine macrophage inflammatory protein-1 α.  J. Immunol. 149:1004 1009.

Sherry B, Yarlett N, Strupp A, Cerami A (1992) Identification of cyclophilin as a pro-inflammatory secretory product of LPS-activated macrophages.  Proc. Natl. Acad. Sci. USA. 89:3511-3515.

Fahey TJ III, Tracey KJ, Tekamp-Olson P, Cousens LS, Jones WG, Shires GT, Cerami A, Sherry B (1992) Macrophage inflammatory protein 1 modulates macrophage function.  J. Immunol. 148:2764-2769.

Broxmeyer HE, Sherry B, Cooper S, Ruscetti FW, Williams DE, Arosio P, Kwon BS, Cerami A (1991) Macrophage inflammatory protein (MIP) 1b abrogates the capacity of MIP 1a to suppress myeloid progenitor cell growth.  J. Immunol.  147:2586-2594.

Widmer U, Yang Z, van Deventer S, Manogue KR, Sherry B, Cerami A (1991) Genomic structure of murine macrophage inflammatory protein (MIP)-1α:  Conservation of potential regulatory sequences with the human homolog LD78.  J. Immunol.   146:4031-4040.

Sherry B and Cerami A (1991) Small cytokine superfamily.  Curr. Opinion Immunol. 3:56-60.

Fahey TJ III, Sherry B, Tracey KJ, van Deventer S, Jones WG II, Minei JP, Morgello S, Shires GT, and Cerami A (1990) Cytokine production in a model of wound healing: The appearance of MIP-1, MIP-2, Cachectin/TNF and IL-1.  Cytokine 2:92-99.

Sherry B, Jue D-M, Zentella A, and Cerami A (1990) Characterization of high molecular weight glycosylated forms of murine cachectin/TNF.  BBRC 173:1072-1078.

Jue D-M, Sherry B, Luedke C, Manogue K, and Cerami A (1990) Processing of newly-synthesized cachectin/tumor necrosis factor in endotoxin-stimulated macrophages.  Biochemistry 29:8371-8377.

Broxmeyer HE, Sherry B, Lu L, Cooper S, Oh K-O, Olson P-T, Kwon BS, and Cerami A (1990) Enhancing and suppressing effects of recombinant murine macrophage inflammatory proteins on colony formation in vitro by bone marrow myeloid progenitor cells.  Blood. 76:1110-1116.

Tekamp-Olson P, Gallegos C, Bauer D, McClain J, Sherry B, Fabre M, van Deventer S, and Cerami A (1990) Cloning and characterization of cDNAs for murine macrophage inflammatory protein-2 and its human homologs.  J. Exp. Med. 172:911-919.

Broxmeyer HE, Sherry B, Lu L, Cooper S, Carow C, Wolpe SD, and Cerami A (1989) Myelopoietic enhancing effects of murine macrophage inflammatory proteins 1 and 2 on colony formation In vitro by murine and human bone marrow granulocyte/macrophage progenitor cells.  J. Exp. Med.  170:1583-1593.

Sherry BA, Gelin F, Fong Y, Marano M, Wei H, Cerami A, and Lowry SF, Lundholm KG, Moldawer LL (1989) Anti-cachectin/tumor necrosis factor-α antibodies attenuate the development of cachexia in two murine transplantable tumor models.   FASEB J.  3:1956-1962.

Davatelis G, Wolpe SD, Sherry B, Dayer J-M, Chicheportiche R, and Cerami A (1989) Macrophage inflammatory protein-1 (MIP-1) is an endogenous pyrogen that acts independently of prostaglandin synthesis.  Science 243:1066-1068.

Wolpe SD, Sherry B, Juers D, Davatelis G, Yurt RW, and Cerami A (1989) Identification and characterization of macrophage inflammatory protein 2.  Proc. Natl. Acad. Sci. USA.  86:612-616.

Sherry B, Tekamp-Olson P, Gallegos C, Bauer D, Davatelis G, Wolpe SD, Masiarz F, Coit D, and Cerami A (1988) Resolution of the two components of macrophage inflammatory protein 1, and cloning and characterization of one of those components, macrophage inflammatory protein 1ß.  J. Exp. Med. 168:2251-2259.

Sherry B, and Cerami A (1988) Cachectin/tumor necrosis factor exerts endocrine, paracrine and autocrine control of inflammatory responses.  J. Cell Biol.  107:1269-1277.

Wolpe SD, Davatelis G, Sherry B, Beutler B, Hesse DG, Nguyen HT, Moldawer LL, Nathan CF, Lowry SF, and Cerami A (1988) Macrophages secrete a novel heparin-binding protein with inflammatory and neutrophil chemokinetic properties.  J. Exp. Med.  167:570-581.