Associate Professor, Medicine, Boston University School of Medicine
Infectious Disease
Dr. Robin R. Ingalls, MD
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Dr. Robin R. Ingalls is an expert in the field of Infectious Disease. She went to medical school at Harvard Medical School. Harvard Medical School is a top medical college. Harvard Medical School is ranked 1/12 in Research/PrimaryCare. Robin Ingalls is also a published doctor. She has 37 paper published. The most recent paper is: CD11/CD18 and CD14 share a common lipid A signaling pathway. Robin Ingalls accepts Medicare payments and is registered with Medicare.gov.
Publications
- The sst1 Resistance Locus Regulates Evasion of Type I Interferon Signaling by Chlamydia pneumoniae as a Disease Tolerance Mechanism.
- Activation of NOD receptors by Neisseria gonorrhoeae modulates the innate immune response.
- CD14 cooperates with complement receptor 3 to mediate MyD88-independent phagocytosis of Borrelia burgdorferi.
- Enhanced Virulence of Chlamydia muridarum Respiratory Infections in the Absence of TLR2 Activation.
- Inflammation and fibrosis during Chlamydia pneumoniae infection is regulated by IL-1 and the NLRP3/ASC inflammasome.
- Mouse strain-dependent differences in susceptibility to Neisseria gonorrhoeae infection and induction of innate immune responses.
- Plasmid-deficient Chlamydia muridarum fail to induce immune pathology and protect against oviduct disease.
- Innate immunity at the mucosal surface: role of toll-like receptor 3 and toll-like receptor 9 in cervical epithelial cell responses to microbial pathogens.
- Localization of TLR2 and MyD88 to Chlamydia trachomatis inclusions. Evidence for signaling by intracellular TLR2 during infection with an obligate intracellular pathogen.
- The Lip lipoprotein from Neisseria gonorrhoeae stimulates cytokine release and NF-kappaB activation in epithelial cells in a Toll-like receptor 2-dependent manner.
- Cellular activation, phagocytosis, and bactericidal activity against group B streptococcus involve parallel myeloid differentiation factor 88-dependent and independent...
- Response to Neisseria gonorrhoeae by cervicovaginal epithelial cells occurs in the absence of toll-like receptor 4-mediated signaling.
- Differential roles of TLR2 and TLR4 in the host response to Gram-negative bacteria: lessons from a lipopolysaccharide-deficient mutant of Neisseria meningitidis.
- Fibroblast growth factor-inducible 14 (Fn14) is expressed in the lower genital tract and may play a role in amplifying inflammation during infection.
- Protective role of Toll-like receptor 4 in experimental gonococcal infection of female mice.
- CD11c/CD18, a transmembrane signaling receptor for lipopolysaccharide.
- The inflammatory cytokine response to Chlamydia trachomatis infection is endotoxin mediated.
- Mycobacterial lipoarabinomannan recognition requires a receptor that shares components of the endotoxin signaling system.
- Binding of Cryptococcus neoformans to heterologously expressed human complement receptors.
- Outside-in signaling by lipopolysaccharide through a tailless integrin.
- Targeted deletion of the lipopolysaccharide (LPS)-binding protein gene leads to profound suppression of LPS responses ex vivo, whereas in vivo responses remain intact.
- CD11/CD18 leukocyte integrins: new signaling receptors for bacterial endotoxin.
- Involvement of CD14 and complement receptors CR3 and CR4 in nuclear factor-kappaB activation and TNF production induced by lipopolysaccharide and group B streptococcal...
- The CD11/CD18 integrins: characterization of three novel LPS signaling receptors.
- Construction of a lipopolysaccharide reporter cell line and its use in identifying mutants defective in endotoxin, but not TNF-alpha, signal transduction.
- CD11/CD18 and CD14 share a common lipid A signaling pathway.
- Membrane expression of soluble endotoxin-binding proteins permits lipopolysaccharide signaling in Chinese hamster ovary fibroblasts independently of CD14.
- Lipopolysaccharide recognition, CD14, and lipopolysaccharide receptors.
- Cutting edge: recognition of Gram-positive bacterial cell wall components by the innate immune system occurs via Toll-like receptor 2.
- Toll-like receptor 2 functions as a pattern recognition receptor for diverse bacterial products.
- Toll-like receptor 4 imparts ligand-specific recognition of bacterial lipopolysaccharide.
- Divergent response to LPS and bacteria in CD14-deficient murine macrophages.
- Involvement of CD14 and beta2-integrins in activating cells with soluble and particulate lipopolysaccharides and mannuronic acid polymers.
- Membrane-associated proteins of a lipopolysaccharide-deficient mutant of Neisseria meningitidis activate the inflammatory response through toll-like receptor 2.
- Induction of tolerance to lipopolysaccharide and mycobacterial components in Chinese hamster ovary/CD14 cells is not affected by overexpression of Toll-like receptors ...
- Comparative analysis of the growth and biological activity of a respiratory and atheroma isolate of Chlamydia pneumoniae reveals strain-dependent differences in inflam...
Schools
Harvard Medical School
Boston University Med Center
Boston University School Med
Doctors Specialties
- Infectious Disease Medicine
- Infectious Disease
Accepted Insurances
Education
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Boston University Medical Center -
Harvard Medical School
Hospital
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Boston Medical Center
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1073590808 |
| Last Name Of The Provider | INGALLS |
| First Name Of The Provider | ROBIN |
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