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Inflammation and Autoimmunity

When our immune system is inappropriately activated this can result in chronic inflammation and autoimmune diseases including ulcerative colitis, rheumatoid arthritis, and multiple sclerosis amongst others. Recent progress in immunology research has expanded our knowledge on immune system's involvement in these diseases, as well as diseases traditionally not perceived as immune-related conditions such as endometriosis and Gaucher’s disease.

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A more in-depth view

The immune system involves a diverse array of specialized cell types, such as T cells, B cells, dendritic cells, monocytes, and macrophages, forming a complex network that collaborates with non-immune cells like fibroblasts. Together, these cells work in tandem, releasing inflammatory mediators that contribute to disease pathology. 

Concept Life Sciences’ expert immunologists can support your immunology programs with a wide selection of services including in vitro immunology assays which model the key facets of inflammatory and autoimmune processes.

Learn how CLS can support your drug discovery program in inflammation and auto-immunity:

  1. Modelling Dendritic Cell Activation:
  • Understanding DC Influence: Aberrant DC activation leads to undesired T cell responses.
  • Utilizing In Vitro Models: Employing monocyte-derived DCs cultured alone or with T cells in varied formats.
  • Assessing Compound Effects: Read-outs include changes in cell-specific marker expression and cytokine production on DCs and T cells. Aim is to downregulate DC activation and mitigate exaggerated T cell responses.
  1. Modelling T Cell Activation:
  • Triggering T Cell Activation: Unwanted T cell activation triggers prolonged pro-inflammatory mediator release.
  • In Vitro Activation Models: Using PBMC or CD3+ T cell cultures activated by TCR triggering or viral peptides.
  • Assessing Compound Impact: Monitoring T cell proliferation, marker expression, and cytokine release to counter T cell activation. Differentiation into distinct T helper cell subsets also assessed.
  1. Modelling Treg Function:
  • Regulating Immune Response: Tregs control immune responses by suppressing helper T cell reactions.
  • Utilizing Suppression Assay: Testing compounds' potential to enhance Treg suppression using nTreg and iTreg co-cultures with responder T cells. Evaluating suppression levels through proliferation or cytokine analysis.
  1. Modelling Macrophage Function:
  • Role of Macrophages: Macrophages contribute to various pathologies and possess plasticity.
  • Generating Distinct Subpopulations: Protocols create immune-activating M1-like and immune-suppressive M2-like macrophages.
  • Assessing Compound Effects: Evaluating compounds' anti-inflammatory function by inducing macrophage transition and assessing cytokine profiles. Additionally, evaluating the impact on T cell activation via macrophage/T-cell co-culture assays.
  1. Modelling Fibroblast Function:
  • Dual Role of Fibroblasts: Fibroblasts play inflammatory roles and recruit immune cells in inflammatory diseases.
  • Using in vitro Assays: Utilizing primary and immortalized fibroblasts from pathogenic tissue to gauge compound effects on proliferation and inflammatory mediator release.
  1. Modelling B Cell Function:
  • Role of B cell: B cells are major effector cells in autoimmunity through antibody production, T cell help and pro-inflammatory cytokine production. 
  • In Vitro Activation Models: From B cell phenotyping and isolation to functional testing – Modulation of B cell activity by test compounds using relevant read-outs such as proliferation, cytokine and antibody secretion and activation markers expression. 

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