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Enzyme-Linked Immunosorbent Assay

Enzyme-Linked Immunosorbent Assay

In 1971, Peter Perlman and Eva Engvall developed an Enzyme-linked immunosorbent assay (ELISA or EIA). ELISA differs from western blot in that the assays are conducted in microtiter plates or in vivo rather than on an absorbent membrane.
There are many different types of ELISAs, but they all involve an antibody molecule whose constant region binds an enzyme, leaving the variable region free to bind its specific antigen. Enzyme-substrate reaction allows the antigen to be visualized or quantified.

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Related Experiment Video

Updated: May 13, 2026

Detection of Antibodies That Neutralize the Cellular Uptake of Enzyme Replacement Therapies with a Cell-based Assay

Detection of Antibodies That Neutralize the Cellular Uptake of Enzyme Replacement Therapies with a Cell-based Assay

Published on: September 10, 2018

Immune surveillance for ERAAP dysfunction.

Niranjana A Nagarajan¹, Nilabh Shastri

¹Division of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720-3200, USA.

Molecular Immunology

|February 26, 2013

Summary

Immune cells detect endoplasmic reticulum aminopeptidase (ERAP1) dysfunction by recognizing novel peptides presented by MHC class Ib molecules. These T cells eliminate ERAP1-deficient cells, highlighting a new immune surveillance pathway.

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Overlapping Peptide Library to Map Qa-1 Epitopes in a Protein

Overlapping Peptide Library to Map Qa-1 Epitopes in a Protein

Published on: December 20, 2017

Related Experiment Videos

Last Updated: May 13, 2026

Detection of Antibodies That Neutralize the Cellular Uptake of Enzyme Replacement Therapies with a Cell-based Assay

Detection of Antibodies That Neutralize the Cellular Uptake of Enzyme Replacement Therapies with a Cell-based Assay

Published on: September 10, 2018

Overlapping Peptide Library to Map Qa-1 Epitopes in a Protein

Overlapping Peptide Library to Map Qa-1 Epitopes in a Protein

Published on: December 20, 2017

Area of Science:

Immunology
Molecular Biology
Cellular Biology

Background:

Endoplasmic reticulum aminopeptidase (ERAP1) trims peptides for MHC class I presentation.
ERAP1 dysfunction is linked to autoimmune diseases and viral inhibition.
Mechanisms for immune detection of ERAP1 defects remain unclear.

Purpose of the Study:

To investigate how the immune system detects ERAP1 dysfunction.
To identify the specific immune response elicited by ERAP1-deficient cells.
To explore the role of MHC class Ib molecules in this process.

Main Methods:

Analysis of peptide-MHC class I (pMHC I) repertoire in ERAP1-deficient cells.
CD8+ T cell response assessment in wild-type (WT) mice.
Identification of novel peptides presented by MHC class Ib molecules.
In vitro and in vivo assays to evaluate T cell-mediated elimination of target cells.

Main Results:

ERAP1-deficient cells present an immunogenic pMHC I repertoire, activating CD8+ T cells.
WT CD8+ T cells recognize peptides presented by MHC class Ib molecules on ERAP1-deficient cells.
FL9 peptide presented by Qa-1(b) on ERAP1-deficient cells was identified.
MHC Ib-restricted CD8+ T cells eliminated ERAAP-deficient cells effectively.
T cells specific for FL9-Qa-1(b) are frequent in naive WT mice and display an antigen-experienced phenotype.

Conclusions:

Novel non-classical pQa-1(b) complexes signal cytotoxic T cells to target cells with ERAP1 defects.
pMHC Ib-specific T cells play a role in immune surveillance for ERAP1 dysfunction.
This pathway offers a new perspective on immune response to peptide-processing defects.