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Cell Migration

Cell Migration

Cell migration, the process by which cells move from one location to another, is essential for the proper development and viability of organisms throughout their life. When cells are not able to migrate properly to their ordained locations, various disorders may occur. For example, disruption in cell migration causes chronic inflammatory diseases such as arthritis.

Cell Migration

Cell Migration

Cell migration is a process by which the cells move from one location to another, playing an essential role in embryological development, repair and regeneration, immune response, and metastasis. Cells migrate in response to chemical or mechanical signals generated by specific organs or tissues. The overall mechanism includes three steps - polarization, protrusion, and release. Polarization involves the formation of a distinct cell front and rear, which determines the direction of movement.

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Related Experiment Video

Updated: Jun 18, 2026

Examining the Role of Nasopharyngeal-associated Lymphoreticular Tissue (NALT) in Mouse Responses to Vaccines

Examining the Role of Nasopharyngeal-associated Lymphoreticular Tissue (NALT) in Mouse Responses to Vaccines

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TNF-alpha regulates corneal Langerhans cell migration.

I Dekaris¹, S N Zhu, M R Dana

¹Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA.

Journal of Immunology (Baltimore, Md. : 1950)

|April 14, 1999

Summary

Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) influence Langerhans cell (LC) migration in the cornea. TNF-alpha

Area of Science:

Ophthalmology
Immunology
Cell Biology

Background:

Langerhans cells (LCs) are crucial for immune responses on the ocular surface.
LC migration into the cornea is vital for conditions like allograft rejection and herpetic keratitis.
The precise molecular mechanisms governing ocular LC migration remain largely unknown.

Purpose of the Study:

To investigate if TNF-alpha mediates corneal LC migration.
To elucidate the interplay between IL-1 and TNF-alpha in regulating LC migratory capacity.
To determine the roles of specific TNF receptor subunits (p55 and p75) in this process.

Main Methods:

Utilized gene-targeted knockout mice lacking IL-1 receptor I (IL-1RI-/-), TNF receptor I (p55-/-), TNF receptor II (p75-/-), or both (p55-/-p75-/-).

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Last Updated: Jun 18, 2026

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Induced LC migration via thermal cautery or intracorneal cytokine injection.

Quantified LC migration using immunofluorescence assays.

Main Results:

LC migration following cauterization or TNF-alpha injection was significantly reduced in p55-/- and p75-/- mice.
Intracorneal IL-1alpha injection led to reduced LC migration in p55-/-, p75-/-, and p55-/-p75-/- mice within 72 hours.
TNF-alpha injection in IL-1RI-/- mice resulted in normal corneal LC migration, indicating IL-1 receptor independence for TNF-alpha-induced migration.

Conclusions:

IL-1-induced corneal LC migration is primarily mediated through TNF receptor (TNFR) signaling.
TNF-alpha-induced LC migration in the cornea operates independently of IL-1 receptor I (IL-1RI) activity.
Both p55 and p75 TNF receptor signaling pathways are essential for mediating LC migration in the cornea.