Adhesion Molecules on the Plasma Membrane of Epidermal Cells. III. Keratinocytes and Langerhans Cells Constitutively Express the Lymphocyte Function-Associated Antigen 3

Panfilis, Giuseppe De; Manara, G. C.; Ferrari, C.; Torresani, Claudio

doi:10.1111/1523-1747.ep12470220

Cited by 26 publications

(12 citation statements)

References 26 publications

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“…Keratinocytes are unable to migrate to draining lymph nodes to present antigen to naïve T cells. Nevertheless, upon exposure to inflammatory stimuli, they produce a variety of cytokines (TNF-α, IL-1, GM-CSF, IL-10) and chemokines, and, in addition, they can express several costimulatory molecules, such as MHC class II, CD54 (intercellular adhesion molecule 1 [ICAM-1]), CD40, and CD58 (LFA-3) [31,32]. Studies with transgenic mice that overexpress B7.1 show that, under this condition, keratinocytes can amplify contact hypersensitivity responses, suggesting that they can promote rather than inhibit T-cell activation when the appropriate second signal is provided [33,34].…”

Section: Costimulatory Moleculesmentioning

confidence: 99%

Keratinocytes in Atopic dermatitis: Inflammatory signals

Esche

Benedetto

Beck

2004

Curr Allergy Asthma Rep

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Atopic dermatitis (AD) is a chronic inflammatory skin disorder that usually predates the development of allergic airway disease. In most cases, this is thought to be an allergen-driven disease with prominent roles played by antigen presenting cells and effector Th2 cells. But keratinocytes, by virtue of their location, provide an important window to the environment and are also thought to contribute to the development of AD. In this review, we discuss several biologic attributes of keratinocytes that are relevant for AD: 1) intrinsic defects in barrier function, 2) production of inflammatory mediators that promote or maintain allergic inflammation, 3) keratinocyte apoptosis, 4) effects of staphylococcal toxins on keratinocytes, and 5) potential consequences of the expression of cosignaling molecules (eg, B7 family members) and receptors important for innate immune responses (eg, Toll receptors). Clearly, these findings have highlighted a more active role played by the epithelium than was previously recognized.

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Section: Costimulatory Moleculesmentioning

confidence: 99%

Keratinocytes in Atopic dermatitis: Inflammatory signals

Esche

Benedetto

Beck

2004

Curr Allergy Asthma Rep

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“…Briefly, bulk EC, suspended in RPMI supplemented with 10% FCS at approximately 5 × 10 6 EC/ml, were prefixed for 10 min at 4°C in 0.1% glutaraldehyde in 0.1 M cacodylate buffer pH 7.4; then 50 mM glycine was used, to quench aldehyde groups. Thus, the time necessary to allow the expression on the LC membrane of CD95‐L in this experiment, as well as of other activation markers in previous experiments (20–22,26,35), was about 3–4 h, namely, from the remotion of skin ex vivo to this prefixation. After washings in PBS‐0.1% BSA, pH 7.2, a blocking pretreatment was carried out, including PBS‐1% BSA, 0.2% sodium azide, and 10% decomplemented human AB serum, for 30 min.…”

Section: Methodsmentioning

confidence: 66%

“…Also, for the P‐E immunostaining the procedure was the same as we used to show surface markers used by activated LC for antigen presentation, i.e. MHC‐class II molecules (15,20), CD54 (21) and CD58 (22) adhesion molecules, CD80 and CD86 co‐stimulatory molecules (our unpublished observations) and the receptor for T‐cell signals CD40 (26). Briefly, bulk EC, suspended in RPMI supplemented with 10% FCS at approximately 5 × 10 6 EC/ml, were prefixed for 10 min at 4°C in 0.1% glutaraldehyde in 0.1 M cacodylate buffer pH 7.4; then 50 mM glycine was used, to quench aldehyde groups.…”

Section: Methodsmentioning

confidence: 99%

The tolerogenic molecule CD95‐L is expressed on the plasma membrane of human activated, but not resting, Langerhans' cells.

Panfilis

Venturini

Llombart‐Bosch³

et al. 2003

Experimental Dermatology

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Although dendritic cells (DC) are well known for their immunogenic capacities, they may even induce peripheral T-cell tolerance, and such a tolerogenic potential can be exerted in mouse through the expression on the DC plasma membrane of the CD95-ligand (CD95-L) molecule, which is able to trigger apoptosis of CD95-expressing antigen-specific T cells. We therefore asked whether epidermal DC, namely Langerhans' cells (LC), either resting (i.e. within the epidermis, 'in situ') or activated (i.e. suspended from the epidermis) or both, could express the CD95-L molecule on the plasma membrane. For such a purpose, two colloidal gold-immunoelectron microscopy (IEM) double-step procedures were carried out: an 'in situ' method, able to investigate resting LC, was performed on ultrathin frozen sections obtained by ultracryomicrotomy (UCMT) of normal skin biopsies; a pre-embedding (P-E) method, able to investigate suspended LC, was performed on epidermal cells (EC) suspended from normal skin specimens. In UCMT/IEM sections, resting LC showed gold particles within the cytoplasm but very rarely within organelles and never along the plasma membrane: resting LC are therefore capable of synthesizing CD95-L but not of expressing it in a functional location, thus autoreactive phenomena against CD95-expressing EC being avoided in normal epidermis. On the other hand, in P-E/IEM preparations, suspended LC showed several gold particles along the plasma membrane: activated LC are therefore capable of expressing CD95-L in a functional location, thus bearing the potential to exert tolerogenic capabilities against CD95-expressing T cells, e.g. to prevent inflammatory/autoimmune cutaneous disorders and/or favor the resolution thereof.

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“…Integrins are a group of mammalian cell surface molecules which can function as receptors for bacterial ligands, promoting bacterial adherence and internalization into mammalian cells [51]. ITGAL combines with ITGB2 to form the integrin LFA-1 (lymphocyte function-associated antigen-1), which is expressed on all leukocytes and resting Langerhan's dendritic cells as well [52]. We had demonstrated previously that blocked α-chain (ITGAL) of the integrin LFA-1, decrease Brucella abortus binding to mononuclear phagocytes [53].…”

Section: Resultsmentioning

confidence: 99%

Systems Biology Analysis of Brucella Infected Peyer's Patch Reveals Rapid Invasion with Modest Transient Perturbations of the Host Transcriptome

et al. 2013

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Brucella melitensis causes the most severe and acute symptoms of all Brucella species in human beings and infects hosts primarily through the oral route. The epithelium covering domed villi of jejunal-ileal Peyer's patches is an important site of entry for several pathogens, including Brucella. Here, we use the calf ligated ileal loop model to study temporal in vivo Brucella-infected host molecular and morphological responses. Our results document Brucella bacteremia occurring within 30 min after intraluminal inoculation of the ileum without histopathologic traces of lesions. Based on a system biology Dynamic Bayesian Network modeling approach (DBN) of microarray data, a very early transient perturbation of the host enteric transcriptome was associated with the initial host response to Brucella contact that is rapidly averted allowing invasion and dissemination. A detailed analysis revealed active expression of Syndecan 2, Integrin alpha L and Integrin beta 2 genes, which may favor initial Brucella adhesion. Also, two intestinal barrier-related pathways (Tight Junction and Trefoil Factors Initiated Mucosal Healing) were significantly repressed in the early stage of infection, suggesting subversion of mucosal epithelial barrier function to facilitate Brucella transepithelial migration. Simultaneously, the strong activation of the innate immune response pathways would suggest that the host mounts an appropriate protective immune response; however, the expression of the two key genes that encode innate immunity anti-Brucella cytokines such as TNF-α and IL12p40 were not significantly changed throughout the study. Furthermore, the defective expression of Toll-Like Receptor Signaling pathways may partially explain the lack of proinflammatory cytokine production and consequently the absence of morphologically detectable inflammation at the site of infection. Cumulatively, our results indicate that the in vivo pathogenesis of the early infectious process of Brucella is primarily accomplished by compromising the mucosal immune barrier and subverting critical immune response mechanisms.

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Adhesion Molecules on the Plasma Membrane of Epidermal Cells. III. Keratinocytes and Langerhans Cells Constitutively Express the Lymphocyte Function-Associated Antigen 3

Cited by 26 publications

References 26 publications

Keratinocytes in Atopic dermatitis: Inflammatory signals

Keratinocytes in Atopic dermatitis: Inflammatory signals

The tolerogenic molecule CD95‐L is expressed on the plasma membrane of human activated, but not resting, Langerhans' cells.

Systems Biology Analysis of Brucella Infected Peyer's Patch Reveals Rapid Invasion with Modest Transient Perturbations of the Host Transcriptome

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