scispace - formally typeset
Search or ask a question
Author

Erwin W. Gelfand

Bio: Erwin W. Gelfand is an academic researcher from University of Colorado Denver. The author has contributed to research in topics: Immunoglobulin E & T cell. The author has an hindex of 99, co-authored 675 publications receiving 36059 citations. Previous affiliations of Erwin W. Gelfand include University of Colorado Hospital & University of Virginia.


Papers
More filters
Journal ArticleDOI
TL;DR: Measurement of AR to inhaled methacholine by barometric whole-body plethysmography is a valid indicator of airway hyperresponsiveness after allergic sensitization in mice, and it is shown that AR measured as Penh was associated with increased IgE production and eosinophil lung infiltration.
Abstract: To study the mechanisms and kinetics underlying the development of increased airway responsiveness (AR) after allergic sensitization, animal models have been invaluable. Using barometric whole-body plethysmography and increases in enhanced pause (Penh) as an index of airway obstruction, we measured responses to inhaled methacholine in conscious, unrestrained mice after sensitization and airway challenge with ovalbumin (OVA). Sensitized and challenged animals had significantly increased AR to aerosolized methacholine compared with control animals. AR measured as Penh was associated with increased IgE production and eosinophil lung infiltration. In a separate approach we confirmed the involvement of the lower airways in the response to aerosolized methacholine using tracheotomized mice. Increases in Penh values after methacholine challenge were also correlated with increased intrapleural pressure, measured via an esophageal tube. Lastly, mice demonstrating AR using a noninvasive technique also demonstrated ...

1,331 citations

Journal ArticleDOI
19 May 1989-Science
TL;DR: The specificity of these toxins for V beta s puts them in the recently described class of superantigens and may account for the differential sensitivity of different individuals to the toxic effects of these proteins.
Abstract: The staphylococcal toxins are responsible for a number of diseases in man and other animals. Many of them have also long been known to be powerful T cell stimulants. They do not, however, stimulate all T cells. On the contrary, each toxin reacts with human T cells bearing particular V beta sequences as part of their receptors for major histocompatibility complex protein-associated antigen. The specificity of these toxins for V beta s puts them in the recently described class of superantigens and may account for the differential sensitivity of different individuals to the toxic effects of these proteins.

722 citations

Journal ArticleDOI
TL;DR: Accumulating evidence is reviewed suggesting that histamine indeed has roles in inflammation and immune function modulation in such diseases and a possible synergy between H1 and H4-receptor antagonists in targeting various inflammatory conditions is reviewed.
Abstract: Histamine has a key role in allergic inflammatory conditions. The inflammatory responses resulting from the liberation of histamine have long been thought to be mediated by the histamine H1 receptor, and H1-receptor antagonists--commonly known as antihistamines--have been used to treat allergies for many years. However, the importance of histamine in the pathology of conditions such as asthma and chronic pruritus may have been underestimated. Here, we review accumulating evidence suggesting that histamine indeed has roles in inflammation and immune function modulation in such diseases. In particular, the discovery of a fourth histamine receptor (H4) and its expression on numerous immune and inflammatory cells has prompted a re-evaluation of the actions of histamine, suggesting a new potential for H4-receptor antagonists and a possible synergy between H1 and H4-receptor antagonists in targeting various inflammatory conditions.

523 citations

Journal ArticleDOI
Antonia Kwan1, Roshini S. Abraham2, Robert Currier, Amy Brower3, Karen Andruszewski4, Jordan K. Abbott5, Mei W. Baker6, Mark Ballow7, Louis Bartoshesky8, Francisco A. Bonilla9, Charles D. Brokopp6, Edward G. Brooks10, Michele Caggana11, Jocelyn Celestin12, Joseph A. Church13, Anne Marie Comeau14, James A. Connelly15, Morton J. Cowan1, Charlotte Cunningham-Rundles16, Trivikram Dasu17, Nina Dave18, Maria Teresa de la Morena19, Ulrich A. Duffner20, Chin-To Fong21, Lisa R. Forbes22, Lisa R. Forbes23, Debra Freedenberg24, Erwin W. Gelfand5, Jaime E. Hale14, I. Celine Hanson22, I. Celine Hanson23, Beverly N. Hay14, Diana Hu, Anthony J. Infante10, Daisy Johnson24, Neena Kapoor13, Denise M. Kay11, Donald B. Kohn25, Rachel Lee24, Heather K. Lehman7, Zhili Lin26, Fred Lorey, Aly Abdel-Mageed20, Adrienne Manning27, Sean A. McGhee28, Sean A. McGhee29, Theodore B. Moore25, Stanley J. Naides30, Luigi D. Notarangelo9, Jordan S. Orange23, Jordan S. Orange22, Sung-Yun Pai9, Matthew H. Porteus29, Matthew H. Porteus28, Ray Rodriguez18, Neil Romberg31, John M. Routes17, Mary Ruehle22, Arye Rubenstein, Carlos A. Saavedra-Matiz11, Ginger Scott24, Patricia M. Scott, Elizabeth Secord22, Christine M. Seroogy6, William T. Shearer23, William T. Shearer22, Subhadra Siegel32, Stacy K. Silvers22, E. Richard Stiehm25, Robert W. Sugerman22, John L. Sullivan14, Susan Tanksley24, Millard L. Tierce22, James W. Verbsky17, Beth Vogel11, Rosalyn Walker18, Kelly Walkovich15, Jolan E. Walter9, Richard L. Wasserman22, Michael S. Watson3, Geoffrey A. Weinberg21, Leonard B. Weiner33, Heather Wood4, Anne B. Yates18, Jennifer M. Puck1 
20 Aug 2014-JAMA
TL;DR: Newborn screening in 11 programs in the United States identified SCID in 1 in 58,000 infants, with high survival, and the usefulness of detection of non-SCID T-cell lymphopenia by the same screening remains to be determined.
Abstract: The purpose of newborn screening is early detection of inborn conditions for which prompt treatments mitigate mortality or irreversible damage. The first heritable immune disorders to which newborn screening has been applied are those that together comprise severe combined immunodeficiency (SCID), caused by defects in any of a diverse group of gene products essential for development of adaptive immunity provided by T and B lymphocytes.1,2 A feature of all SCID is defective production of T cells. In most SCID, B cells are also defective, but even normal B cells cannot produce antibodies without T-cell help. Thus, infants with SCID are susceptible to life-threatening infections. Early detection and treatment optimize survival.3-5 Provided that SCID is diagnosed before infections become overwhelming, affected infants can be rescued with hematopoietic stem cell transplantation; gene therapy; or, for adenosine deaminase deficiency, enzyme replacement therapy.2,5-8 Population-based screening is the only means to detect SCID prior to the onset of infections in most cases, as more than 80% lack a positive family history.9,10 T-cell receptor excision circles (TRECs), a biomarker for T lymphopoiesis,11 can be measured by polymerase chain reaction (PCR) using DNA isolated from infant dried blood spots collected for newborn screening.9 Dried blood spots from apparently healthy newborns who were later diagnosed with SCID lacked TRECs.9 Confirmation of the utility of the TREC test,12 adaptation for pilot newborn screening programs in Wisconsin13 and Massachusetts,14 and an evidence-based review led to the recommendation by the US Department of Health and Human Services Secretary in 2010 that SCID be added to the Uniform Screening Panel for all newborns, with related T-cell deficiencies added to the list of secondary targets.15 Currently, 23 states, the District of Columbia, and the Navajo Nation screen approximately two-thirds of all infants born in the United States for SCID. Individual states have confirmed detection of SCID as well as additional disorders with low T-cell numbers, which also may benefit from further assessment of immune dysfunction and from protective treatments.13,16-18 Here we present the first combined analysis of more than 3 million infants screened for SCID in 10 states and the Navajo Nation, providing a population-based overview of SCID and non-SCID T-cell lymphopenia.

512 citations

Journal ArticleDOI
TL;DR: It is demonstrated that lung-specific IL-5 expression can induce pathologic changes characteristic of asthma and may provide useful models to evaluate the efficacy of potential respiratory disease therapies or pharmaceuticals.
Abstract: We have generated transgenic mice that constitutively express murine interleukin (IL)-5 in the lung epithelium. Airway expression of this cytokine resulted in a dramatic accumulation of peribronchial eosinophils and striking pathologic changes including the expansion of bronchusassociated lymphoid tissue (BALT), goblet cell hyperplasia, epithelial hypertrophy, and focal collagen deposition. These changes were also accompanied by eosinophil infiltration of the airway lumen. In addition, transgenic animals displayed airway hyperresponsiveness to methacholine in the absence of aerosolized antigen challenge. These findings demonstrate that lung-specific IL-5 expression can induce pathologic changes characteristic of asthma and may provide useful models to evaluate the efficacy of potential respiratory disease therapies or pharmaceuticals.

512 citations


Cited by
More filters
Journal ArticleDOI
TL;DR: It is important that the medical profession play a significant role in critically evaluating the use of diagnostic procedures and therapies as they are introduced in the detection, management, and management of diseases.
Abstract: PREAMBLE......e4 APPENDIX 1......e121 APPENDIX 2......e122 APPENDIX 3......e124 REFERENCES......e124 It is important that the medical profession play a significant role in critically evaluating the use of diagnostic procedures and therapies as they are introduced in the detection, management,

8,362 citations

Journal ArticleDOI
TL;DR: Findings that have advanced the understanding of IL-10 and its receptor are highlighted, as well as its in vivo function in health and disease.
Abstract: Interleukin-10 (IL-10), first recognized for its ability to inhibit activation and effector function of T cells, monocytes, and macrophages, is a multifunctional cytokine with diverse effects on most hemopoietic cell types. The principal routine function of IL-10 appears to be to limit and ultimately terminate inflammatory responses. In addition to these activities, IL-10 regulates growth and/or differentiation of B cells, NK cells, cytotoxic and helper T cells, mast cells, granulocytes, dendritic cells, keratinocytes, and endothelial cells. IL-10 plays a key role in differentiation and function of a newly appreciated type of T cell, the T regulatory cell, which may figure prominently in control of immune responses and tolerance in vivo. Uniquely among hemopoietic cytokines, IL-10 has closely related homologs in several virus genomes, which testify to its crucial role in regulating immune and inflammatory responses. This review highlights findings that have advanced our understanding of IL-10 and its receptor, as well as its in vivo function in health and disease.

6,308 citations

Book ChapterDOI
01 Jan 2010

5,842 citations