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Immune Cell Characterisation

Unlike the innate immune system, the adaptive immune system specifically targets a pathogen with a tailored response.

The adaptive immune system also “remembers” each specific pathogen that it encounters, leading to and creates immunological memory after an initial response to a specific pathogen, this leads to an enhanced response in subsequent encounters with that pathogen. This process of acquired immunity is also the basis of vaccination. The adaptive immune system consists of both cell-mediated and humoral-mediated responses. The two different responses are controlled by two different classes of lymphocytes. T Cells produce the cell mediated response and B Cells produce the humoral (antibody response).

There are many different subsets of T Cells, which can be characterised by both their expression of different markers on their surface, as well as the cytokines that they secrete. The most important cytokines secreted by different T Cell subsets are shown in the adjacent table.

T helper type 1 (Th1) cells

IFN-gamma

T helper type 2 (Th2) cells

IL-4

T helper type 9 (Th9) cells

IL-9

T helper type 17 (Th17) cells

IL-17

T helper type 22 (Th22) cells

IL-22

Follicular helper T (Tfh) cells

IL-21

Regulatory T (Treg) cells

Galectin 1

Natural killer T (NKT) cells

GM-CSF

Gamma delta T cells

Granzyme A/B

CD8+ cytotoxic T lymphocytes (CTLs)

IFN-gamma

Co-Signalling molecules and T Cell activation.

T cell activation requires two signals: The first is recognition of the antigenic peptide bound to the major histocompatibility complex (MHC) by the T cell receptor (TCR). The second signal is independent of antigen, and is provided by interactions between co-signalling molecules expressed on antigen-presenting cells (APCs) and their receptors on the T Cell surface. Activation of the TCR in the absence of this second co-stimulatory signal typically results in T cell anergy or apoptosis. In addition, T cell activation can be supressed by co-inhibitory molecules present on APCs. The integration of the positive and negative signals provided by co-stimulatory and co-inhibitory molecules following TCR engagement directs the outcome and magnitude of the target T cell’s response. This response can be the enhancement or suppression of T cell proliferation, T Cell differentiation, and/or cytokine secretion. Most co-stimulatory and co-inhibitory molecules belong to either the Immunoglobulin (Ig) superfamily or Tumor Necrosis Factor (TNF) receptor superfamily. Immunoglobulin family members are further classified as members of the B7/CD28, butyrophilin, CD2/SLAM, TIM, or nectin- and nectin-like binding receptor subfamilies. TNF receptor superfamily members are classified into the type L or type V subfamilies.

R&D Systems offers an unparalleled selection of recombinant proteins that can be used to characterize the effects of T cell co-signalling molecules.

linkLearn more about Co-stimulatory and Co-inhibitory Molecules

Metabolic Profiling for Immune Cell Profiling

An emerging theme in immunology is that metabolic reprogramming and lymphocyte function are intricately linked. However, why T Cells adopt specific metabolic programs, and the impact that these programs have on T Cells function and, ultimately, immunological outcomes remain unclear. Memory and naïve T Cells face challenges upon activation; they must transition from a quiescent state to a higher energy utilisation state with demands on both their anabolic and catabolic metabolism. Activated T Cells must proliferate quickly while simultaneously producing a range of cytokines to fight infection. Using the Seahorse Extracellular flux analyser, researchers have discovered that T cells regulate their metabolism in response to both immune stimuli and environmental cues. 

Using the Seahorse Energy Phenotyping kit will yield valuable information on how energy utilisation in different immune systems cells changes in response to an increased energy demand. For example Kramer et al showed that lymphocytes will switch to a glycolytic phenotype when their oxidative phosphorylation is blocked, while neutrophils are unaffected by the same block.

pdfDownload Cell Metabolism Assays for Immunology Research
linkRegister for a Seahorse XFp demo here

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18.01.2017