Complementary methods for contact hypersensitivity (CHS) evaluation in mice

Zemelka‐Wiącek, Magdalena; Majewska‐Szczepanik, Monika; Pyrczak, Wieslaw; Szczepanik, Marian

doi:10.1016/j.jim.2012.11.004

Cited by 18 publications

(19 citation statements)

References 18 publications

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“…In CS and DTH, the newly uncovered early 2‐h Ag‐specific peak is due to sB‐1a–derived IgM Ab and/or to Ab FLCs that are evident macroscopically by 2 hours after Ag challenge . Thus, after this second Ag challenge to test skin responsiveness induced by primary immunization, the early response is elicited and which can be quantitated by measurement of ear swelling and by Evans blue vascular permeability; continued measurement reveals the 24–48 h late component of ear skin swelling due to local inflammation . The early 2‐h peak has become an invariable marker of early initiating sB‐1a cells that are required for the subsequent late classical 24–48 h T cell–mediated inflammatory ear swelling .…”

Section: A Role For Sb‐1a Cell–derived Ab Free Light Chains In Murine Csmentioning

confidence: 99%

A subset of AID‐dependent B‐1a cells initiates hypersensitivity and pneumococcal pneumonia resistance

Askenase

Bryniarski

Paliwal

et al. 2015

Annals of the New York Academy of Sciences

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We propose that there is a special B-1a B cell subset (“sB-1a” cells) that mediates linked processes very early after immunization to initiate cutaneous contact sensitivity (CS), delayed-type hypersensitivity (DTH), and immune resistance to pneumococcal pneumonia. Our published data indicate that in CS and DTH these initiating processes are required for elicitation of the delayed onset and late-occurring classical T cell–mediated responses. sB-1a cells resemble memory B2 cells, as they are stimulated within 1-hour of immunization and depend on T helper cytokines—uniquely IL-4 from hepatic iNKT cells–for activation and rapid migration from the peritoneal cavity to the spleen to secrete IgM antibody (Ab) and Ab-derived free light chains (FLC) by only one day after immunization. Unlike conventional B-1a (cB-1a) cell–produced IgM natural Ab, IgM Ab produced by sB-1a cells has high Ag affinity owing to immunoglobulin V-region mutations induced by activation-induced cytidine deaminase (AID). The dominant cB-1a cells are increased in immunized AID-deficient mice but do not mediate initiation, CS, or pneumonia resistance because natural Ab has relatively low Ag-affinity because of unmutated germ line V-regions. In CS and DTH, sB-1a IgM Ag affinity is sufficiently high to mediate complement activation for generation of C5a that, together with vasoactive mediators such as TNF-α released by FLC-sensitized mast cells activate local endothelium for extravascular recruitment of effector T cells. We conclude by discussing the possibility of functional sB-1 cells in humans.

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Section: A Role For Sb‐1a Cell–derived Ab Free Light Chains In Murine Csmentioning

confidence: 99%

A subset of AID‐dependent B‐1a cells initiates hypersensitivity and pneumococcal pneumonia resistance

Askenase

Bryniarski

Paliwal

et al. 2015

Annals of the New York Academy of Sciences

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“…Naive or sMRBC‐tolerized mice were actively contact sensitized and 5 days later challenged with picryl chloride (PCL, Chemtronix) as described elsewhere . After 24 hours, ear swelling was measured with an engineer's micrometre (Mitutoyo) by a blinded observer . Background non‐specific increases in ear thickness in non‐sensitized, but similarly challenged, littermates were subtracted from experimental groups to yield a net swelling value expressed as delta ± standard error (SE) [U × 10 −2 mm].…”

Section: Methodsmentioning

confidence: 99%

Syngeneic red blood cell–induced extracellular vesicles suppress delayed‐type hypersensitivity to self‐antigens in mice

Nazimek

Bustos‐Morán

Blas‐Rus

et al. 2019

Clin Experimental Allergy

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Background At present, the role of autologous cells as antigen carriers inducing immune tolerance is appreciated. Accordingly, intravenous administration of haptenated syngeneic mouse red blood cells (sMRBC) leads to hapten‐specific suppression of contact hypersensitivity (CHS) in mice, mediated by light chain‐coated extracellular vesicles (EVs). Subsequent studies suggested that mice intravenously administered with sMRBC alone may also generate regulatory EVs, revealing the possible self‐tolerogenic potential of autologous erythrocytes. Objectives The current study investigated the immune effects induced by mere intravenous administration of a high dose of sMRBC in mice. Methods The self‐tolerogenic potential of EVs was determined in a newly developed mouse model of delayed‐type hypersensitivity (DTH) to sMRBC. The effects of EV's action on DTH effector cells were evaluated cytometrically. The suppressive activity of EVs, after coating with anti‐hapten antibody light chains, was assessed in hapten‐induced CHS in wild‐type or miRNA‐150−/− mice. Results Intravenous administration of sMRBC led to the generation of CD9 + CD81+ EVs that suppressed sMRBC‐induced DTH in a miRNA‐150‐dependent manner. Furthermore, the treatment of DTH effector cells with sMRBC‐induced EVs decreased the activation of T cells but enhanced their apoptosis. Finally, EVs coated with antibody light chains inhibited hapten‐induced CHS. Conclusions and Clinical Relevance The current study describes a newly discovered mechanism of self‐tolerance induced by the intravenous delivery of a high dose of sMRBC that is mediated by EVs in a miRNA‐150‐dependent manner. This mechanism implies the concept of naturally occurring immune tolerance, presumably activated by overloading of the organism with altered self‐antigens.

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“…Ear punches were transferred to tubes containing 1 ml of formamid. After 18 h incubation at 37°C the samples were centrifuged and the optical density (OD) of Evens blue in the supernatant was read at 565 nm against blank containing formamid [20]. …”

Section: Methodsmentioning

confidence: 99%

“…Neutrophil infiltration to the inflamed ears was indirectly quantitated using a MPO assay, as described previously [20]. Ears were removed 24 h post challenge and 6 mm diameter punch of the ear was made.…”

Section: Methodsmentioning

confidence: 99%

Epicutaneous Immunization with TNP-Ig and Zymosan Induces TCRαβ+ CD4+ Contrasuppressor Cells That Reverse Skin-Induced Suppression via IL-17A

Majewska‐Szczepanik

Strzępa²,

Marcińska³

et al. 2014

Int Arch Allergy Immunol

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Background: Our previous work showed that epicutaneous (EC) immunization with protein antigen e.g. TNP-conjugated mouse immunoglobulin (TNP-Ig) in the form of a patch prior to hapten sensitization inhibits Th1-mediated contact hypersensitivity (CHS) in mice. We also found that suppression of CHS was mediated by TCRαβ+ CD4+ CD8+ T suppressor cells producing TGF-β. The aim of this study was to investigate the role of innate immunity in the suppression of CHS. Methods: Mice were immunized by applying gauze patches containing protein antigen alone or in the presence of zymosan, and were then tested for the CHS response. Adoptive cell transfer experiments were used to study the mechanisms involved in the reversal of skin-induced suppression. The influence of EC immunization on cytokine production by lymph node cells was measured by ELISA. Results: We found that EC immunization with TNP-Ig and zymosan before trinitrophenyl chloride sensitization reverses skin-induced suppression, demonstrated in vivo and in vitro. The reversal of skin-induced suppression was transferable by antigen-specific TCRαβ+ CD4+ T contrasuppressor cells. Furthermore, we showed that the contrasuppression was IL-17A-dependent and TLR2- and MyD88-independent. Conclusions: Our work strongly suggests that EC immunization with protein antigen and zymosan reverses skin-induced suppression and that this approach may be a potential tool to increase the immunogenicity of weakly immunogenic antigens.

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Complementary methods for contact hypersensitivity (CHS) evaluation in mice

Cited by 18 publications

References 18 publications

A subset of AID‐dependent B‐1a cells initiates hypersensitivity and pneumococcal pneumonia resistance

A subset of AID‐dependent B‐1a cells initiates hypersensitivity and pneumococcal pneumonia resistance

Syngeneic red blood cell–induced extracellular vesicles suppress delayed‐type hypersensitivity to self‐antigens in mice

Epicutaneous Immunization with TNP-Ig and Zymosan Induces TCRαβ+ CD4+ Contrasuppressor Cells That Reverse Skin-Induced Suppression via IL-17A

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