scholarly journals Allergic Reactions to Serine Protease-Like Proteins of Staphylococcus aureus

2021 ◽  
Vol 12 ◽  
Author(s):  
Maria Nordengrün ◽  
Goran Abdurrahman ◽  
Janina Treffon ◽  
Hannah Wächter ◽  
Barbara C. Kahl ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
T Cells ◽  
Serine Protease ◽  
Allergic Inflammation ◽  
Allergic Airway Inflammation ◽  
Serum Ige ◽  
Airway Infections ◽  
Type 2 Cytokines ◽  
Type 3

In cystic fibrosis (CF) infectious and allergic airway inflammation cause pulmonary exacerbations that destroy the lungs. Staphylococcus aureus is a common long-term colonizer and cause of recurrent airway infections in CF. The pathogen is also associated with respiratory allergy; especially the staphylococcal serine protease-like proteins (Spls) can induce type 2 immune responses in humans and mice. We measured the serum IgE levels specific to 7 proteases of S. aureus by ELISA, targeting 5 Spls (76 CF patients and 46 controls) and the staphopains A and B (16 CF patients and 46 controls). Then we compared cytokine release and phenotype of T cells that had been stimulated with Spls between 5 CF patients and 5 controls. CF patients had strongly increased serum IgE binding to all Spls but not to the staphopains. Compared to healthy controls, their Spl-stimulated T cells released more type 2 cytokines (IL-4, IL-5, IL-13) and more IL-6 with no difference in the secretion of type 1- or type 3 cytokines (IFNγ, IL-17A, IL-17F). IL-10 production was low in CF T cells. The phenotype of the Spl-exposed T cells shifted towards a Th2 or Th17 profile in CF but to a Th1 profile in controls. Sensitization to S. aureus Spls is common in CF. This discovery could explain episodes of allergic inflammation of hitherto unknown causation in CF and extend the diagnostic and therapeutic portfolio.

scholarly journals A type 2 cytokine axis for thymus emigration

2017 ◽  
Vol 214 (8) ◽  
pp. 2205-2216 ◽  
Author(s):  
Andrea J. White ◽  
Song Baik ◽  
Sonia M. Parnell ◽  
Amanda M. Holland ◽  
Frank Brombacher ◽  
...  
Keyword(s):  
T Cells ◽  
Stromal Cells ◽  
Perivascular Spaces ◽  
Thymocyte Development ◽  
Invariant Nkt Cells ◽  
Developmental Program ◽  
Innate T Cells ◽  
Type 2 Cytokines ◽  
Thymic Stromal Cells

In the thymus, stromal microenvironments support a developmental program that generates mature T cells ready for thymic exit. The cellular and molecular specialization within thymic stromal cells that enables their regulation of specific stages of thymocyte development is poorly understood. Here, we show the thymic microenvironment expresses the type 2 IL-4R complex and is functionally responsive to its known ligands, IL-4 and IL-13. Absence of IL-4Rα limits thymocyte emigration, leading to an intrathymic accumulation of mature thymocytes within medullary perivascular spaces and reduced numbers of recent thymic emigrants. Thymus transplantation shows this requirement maps to IL-4Rα expression by stromal cells, and we provide evidence that it regulates thymic exit via a process distinct from S1P-mediated migration. Finally, we reveal a cellular mechanism by which IL-4+IL-13+ invariant NKT cells are necessary for IL-4Rα signaling that regulates thymic exit. Collectively, we define a new axis for thymic emigration involving stimulation of the thymic microenvironment via type 2 cytokines from innate T cells.

T cells specific for Candida albicans antigens and producing type 2 cytokines in lesional mucosa of untreated HIV-infected patients with pseudomembranous oropharyngeal candidiasis

2008 ◽  
Vol 10 (2) ◽  
pp. 166-174 ◽  
Author(s):  
Alessandra Vultaggio ◽  
Letizia Lombardelli ◽  
Maria Grazia Giudizi ◽  
Roberta Biagiotti ◽  
Benedetta Mazzinghi ◽  
...  
Keyword(s):  
T Cells ◽  
Candida Albicans ◽  
Oropharyngeal Candidiasis ◽  
Type 2 Cytokines

scholarly journals Characteristics of hospital- and community-acquired meticillin-resistant Staphylococcus aureus in Tehran, Iran

2014 ◽  
Vol 63 (6) ◽  
pp. 796-804 ◽  
Author(s):  
Fateh Rahimi ◽  
Mohammad Katouli ◽  
Mohammad Reza Pourshafie
Keyword(s):  
Staphylococcus Aureus ◽  
Multiplex Pcr ◽  
Outpatient Clinic ◽  
Pcr Assay ◽  
Type Iii ◽  
Multiplex Pcr Assay ◽  
Type 3 ◽  
Hospital Acquired ◽  
Staphylococcal Cassette Chromosome

Staphylococcus aureus is a leading cause of hospital-acquired (HA) and community-acquired (CA) infections worldwide. Recently, S. aureus strains resistant to meticillin (MRSA) have become established within both communities. We isolated 314 isolates of MRSA from hospitalized patients in a referral hospital (HA isolates) and 268 isolates from its outpatient clinic (CA isolates) in Tehran, Iran, between February 2008 and December 2010. These isolates were tested for their susceptibility to 17 antibiotics and typed using the PhPlate system. The diversity in the structures of staphylococcal cassette chromosome mec (SCCmec) elements and ccr types was also detected using a multiplex-PCR assay and isolates were examined for the presence of different classes of prophages. Whilst all isolates were resistant to penicillin, the HA isolates were significantly more resistant to all other antibiotics tested than the CA isolates. Isolates carrying only SCCmec type III and ccr type 3 were dominant (91 %), but 20 % of the CA isolates belonging to less prevalent types carried only SCCmec types IVa, c and ccr type 2. These isolates also carried pvl genes and contained SGA prophage type. Our results indicate that whilst the dominant clonal groups of HA- and CA-MRSA belong to SCCmec type III and carry ccr type 3 genes, several distinct but less prevalent types of CA-MRSA carrying SCCmec type IVa, c and type 2 ccr are also found in Tehran. These strains carry pvl genes and the SGA prophage type, a characteristic that might be used as a marker for detection of CA–MRSA in this country.

Peyer's patch CD8+ memory T cells secrete T helper type 1 and type 2 cytokines and provide help for immunoglobulin secretion

1994 ◽  
Vol 24 (12) ◽  
pp. 3087-3092 ◽  
Author(s):  
Anand S. Lagoo ◽  
John H. Eldridge ◽  
Sandhya Lagoo-Deenadaylan ◽  
C. Allen Black ◽  
Ben U. Ridwan ◽  
...  
Keyword(s):  
T Cells ◽  
Memory T Cells ◽  
T Helper ◽  
Peyer's Patch ◽  
Immunoglobulin Secretion ◽  
Type 2 Cytokines ◽  
Cd8 Memory T Cells ◽  
Helper Type

scholarly journals Dysregulated Synthesis of Intracellular Type 1 and Type 2 Cytokines by T Cells of Patients with Cutaneous T-Cell Lymphoma

1999 ◽  
Vol 6 (1) ◽  
pp. 79-84 ◽  
Author(s):  
Bang-Ning Lee ◽  
Madeleine Duvic ◽  
Chih-Kwang Tang ◽  
Carlos Bueso-Ramos ◽  
Zeev Estrov ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Lymphoma ◽  
Study Groups ◽  
Cutaneous T Cell Lymphoma ◽  
Healthy Donors ◽  
Type 2 Cytokines ◽  
Ifn Γ

ABSTRACT Mycosis fungoides (MF) and Sezary syndrome (SS) are the two main clinical entities of cutaneous T-cell lymphoma (CTCL). As the disease progresses from MF to SS, a switch from a type 1 (interleukin [IL]-2 and gamma interferon [IFN-γ]) to a type 2 (IL-4) cytokine production profile occurs. Although roles for type 1 and type 2 cytokines in the pathogenesis of CTCL have been proposed, the cellular origins of these cytokines are unclear. Using flow cytometry to identify individual T-cell subsets, we studied cytokine synthesis by the T cells of 13 patients with SS and 12 with MF and 9 hematologically healthy donors. Upon activation with phorbol 12-myristate 13-acetate (PMA), the numbers of T cells synthesizing IL-2 were similar for all study groups. Whereas the predominant T-cell producing IL-2 in healthy donors and in those with MF was CD7+, in patients with SS, it was CD7−. Although the number of IL-4+CD4+ T cells was low for all study groups, there was a significantly higher number of IL-4+ CD8+ T cells in patients with MF than in those with SS or healthy donors. There was a decline in the number of IFN-γ-producing T cells in CTCL donors compared to that in healthy donors. More importantly, there was a significant decrease in the number of IFN-γ-producing T cells with disease progression from MF to SS. The inability of these T cells to synthesize IFN-γ may have prognostic value in CTCL, since it may be responsible for the progression of the disease from MF to SS.

scholarly journals Spatial and temporal regulation of cytokine expression in Type 2 immune responses

2021 ◽  
Author(s):  
◽  
Ryan Kyle
Keyword(s):  
T Cells ◽  
Lymph Node ◽  
Immune Responses ◽  
Cd4 T Cells ◽  
Helminth Infection ◽  
Allergic Inflammation ◽  
Nippostrongylus Brasiliensis ◽  
Reporter Mice

<p>Type 2 immune responses are generated to provide protection against parasitic helminth infections, however these responses also cause the pathologies associated with allergic inflammation. Studies of the cell types and signalling pathways that mediate Type 2 immune responses have been previously undertaken with the goals of efficient development of vaccines against helminths, and identification of pathways that can be inhibited to decrease the damage caused by allergic inflammation.  The cytokines interleukin-4 (IL-4) and interleukin-13 (IL-13) mediate many of the downstream effector functions of the Type 2 immune response. To study the mechanisms that control expression of these two cytokines I have used a novel dual cytokine IL-4 and IL-13 transgenic reporter mouse. Utilising this tool along with other IL-4 reporter mice I have discovered that the amount of T cell receptor (TCR) signalling modulates the allelic expression of IL-4 by CD4⁺ T cells. The transgenic IL-4 reporter mouse has for the first time allowed independent measurement of the effects of IL-4 deficiency on the expression of IL-4 in vivo. Using this system I have found that IL- 4 is not required for the in vivo generation or expansion of IL-4 producing CD4⁺ T cells. Th2 differentiated CD4⁺ T cells also expresses IL-13, however the dual reporter mice have demonstrated that IL-13 is expressed consistently later than IL-4 in vitro, and IL-13 requires constant, or multiple exposures to TCR stimulus for expression to be induced. IL-13 expression is absent from lymph node CD4⁺ T cells during exposure to allergens or helminth infection. Sequestration of CD4⁺ T cells in the lymph node does not impact the number of IL-13 expressing CD4⁺ T cells in the lung during a helminth infection, indicating that adaptive immune cell derived IL-13 may be entirely produced by lung resident cells not requiring transit through the lymph node.  I have characterised a population of innate lymphoid cells (ILCs) within the skin and found that the proportion of these cells that constitutively express IL-13 decreases with age. These cells did not drastically change in numbers or IL-13 responses in a range of inflammatory conditions including a model of atopic dermatitis. Basophils were found to respond to the atopic dermatitis model by migrating specifically to the treated skin site and draining lymph node, and producing IL-4 in a thymic stromal lymphopoietin dependant manner.  Treatment with exogenous cytokines induced IL-13 expression from group 2 ILCs (ILC2s) in the lung and these cells promoted protective immune responses against Nippostrongylus brasiliensis infection. The immune response generated during a primary infection by Nippostrongylus brasiliensis provides protection from re-infection. Long-term protection is dependent on CD4⁺ T cells but when sufficiently stimulated by cytokine, ILC2s can rescue the protection lost by the depletion of CD4⁺ T cells.  This thesis has shown that CD4⁺ T cells and populations of innate immune cells differentially regulate the expression of the closely related Type 2 cytokines IL-4 and IL- 13. These discoveries will help direct future research aiming to boost the effectiveness of anti-helminth vaccines, or decrease the pathology caused by allergic diseases by targeting specific cytokine expression.</p>

scholarly journals Correction: Human CD141+ Dendritic Cells Induce CD4+ T Cells To Produce Type 2 Cytokines

2014 ◽  
Vol 193 (12) ◽  
pp. 6210-6210 ◽  
Author(s):  
Chun I. Yu ◽  
Christian Becker ◽  
Patrick Metang ◽  
Florentina Marches ◽  
Yuanyuan Wang ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Cd4 T Cells ◽  
Type 2 Cytokines
Sign in / Sign up

Export Citation Format

Share Document