[5] Upon binding to the LTβ receptor, LT-αβ transmits signals leading to proliferation, homeostasis and activation of tissue cells in secondary lymphoid organs through induced expression of chemokines, major histocompatibility complex, and adhesion molecules.
[6][7] Studies have found that mice with an inactivated LT-α gene (LTA) lack developed Peyer's patches and lymph nodes.
[2] Signaling of the LT-β receptors can also induce the differentiation of NK (natural killer) and NK-T cells, which are key players in the innate immune defense and in antiviral responses.
[11] Studies using mice with an LT-α knockout found increased tumor growth in the absence of LT-αβ.
[4][11][13] Mutations in the regulatory factors involved in lymphotoxin signaling may increase the risk of cancer development.
[13] One major instance is the continuous initiation of the NF-κB pathway due to an excessive binding of the LT-α1-β2 complex to LT-β receptors, which can lead to specific cancerous conditions including multiple myeloma and melanoma.