L
Laura Haynes
Researcher at University of Connecticut
Publications - 131
Citations - 9170
Laura Haynes is an academic researcher from University of Connecticut. The author has contributed to research in topics: Immune system & T cell. The author has an hindex of 43, co-authored 109 publications receiving 8268 citations. Previous affiliations of Laura Haynes include University of Rochester Medical Center & University of Porto.
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Journal ArticleDOI
IL-23 and IL-17 in the establishment of protective pulmonary CD4 + T cell responses after vaccination and during Mycobacterium tuberculosis challenge
Shabaana A. Khader,Guy K. Bell,John E. Pearl,Jeffrey J. Fountain,Javier Rangel-Moreno,Garth E Cilley,Fang Shen,Sheri M. Eaton,Sarah L. Gaffen,Susan L. Swain,Richard M. Locksley,Laura Haynes,Troy D. Randall,Andrea M. Cooper +13 more
TL;DR: It is proposed that vaccination induces IL-17-producing CD4+ T cells that populate the lung and, after challenge, trigger the production of chemokines that recruit CD4- T cells producing interferon-γ, which ultimately restrict bacterial growth.
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Reciprocal regulation of polarized cytokine production by effector B and T cells.
David P. Harris,Laura Haynes,Peter C. Sayles,Debra K. Duso,Sheri M. Eaton,Nancy M. Lepak,Lawrence L. Johnson,Susan L. Swain,Frances E. Lund +8 more
TL;DR: Two populations of “effector” B cells (Be1 and Be2) are identified that produce distinct patterns of cytokines depending on the cytokine environment in which the cells were stimulated during their primary encounter with antigen and T cells, suggesting that B cells may regulate immune responses to infectious pathogens through their production of cytokine.
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The induction of antibody production by IL-6 is indirectly mediated by IL-21 produced by CD4+ T cells.
Oliver Dienz,Sheri M. Eaton,Jeffrey P. Bond,Wendy A. Neveu,David Moquin,Rajkumar Noubade,Eva M. Briso,Colette Charland,Warren J. Leonard,Gennaro Ciliberto,Cory Teuscher,Laura Haynes,Mercedes Rincon +12 more
TL;DR: It is shown that IL-6 is sufficient and necessary to induce IL-21 production by naive and memory CD4+ T cells upon T cell receptor stimulation and could be a potential coadjuvant to enhance humoral immunity.
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Interferon γ Eliminates Responding Cd4 T Cells during Mycobacterial Infection by Inducing Apoptosis of Activated Cd4 T Cells
TL;DR: IFN-γ is essential to a regulatory mechanism that eliminates activatedCD4 T cells and maintains CD4 T cell homeostasis during an immune response and was abolished by depleting adherent cells or Mac-1+ spleen cells or by inhibiting nitric oxide synthase.
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Age-related defects in CD4 T cell cognate helper function lead to reductions in humoral responses.
TL;DR: Age-related reductions in the cognate helper function of CD4 T cells contribute significantly to defects in humoral responses observed in aged individuals, and a novel adoptive transfer model is used to compare identical numbers of antigen-specific naive T cells from young and aged TCR transgenic donors.