Numerous studies have demonstrated the critical involvement of hepatic macrophages, including resident Kupffer cells (KCs) and recruited monocyte-derived macrophages, in NASH.1

T2D is characterized by insulin resistance and impaired insulin secretion from pancreatic β-cells. Inflammation plays a key role in the development of β-cell dysfunction. Inflammatory changes, including accumulation of macrophages, have been documented in T2D islets.2

The inflammatory cytokine storm in COVID-19 is thought to be primarily mediated by macrophages.3

Secretion of TGF-β is induced by monocyte [macrophage] activation.4

TGF-β is known to induce IgA isotype class switch, and levels of TGF-beta in COVID-19 patients are associated with increased risk of severity of COVID-19.5

In hospitalized patients with confirmed coronavirus disease COVID-19 only IgA levels were statistically significantly correlated with critical disease regardless of age, sex, and duration of symptoms.6

In “A Review of Persistent Post‑COVID Syndrome”, it is noted that pathologic fibrosis of organs and vasculature leads to increased mortality and severely worsened quality of life. Inhibiting TGF-β, an immuno- and a fibrosis modulator, may attenuate these post-COVID sequelae.7

In a mouse model of post-COVID vaccination myocarditis, immunohistochemical staining indicated increased number of intracardial macrophages or histiocytes positive for CD68.8


1 Cellular & Molecular Immunology 2021 volume 18, 2059–2060.

2 Diabetes Obes Metab. 2013 Sep;15 Suppl 3:152-8.

3 PNAS September 21, 2021 118 (38) e2101071118.

4 Proc. Natl. Acad. Sci. USA 1987 Vol. 84, pp. 6020-6024.

5 J FEBS Letters 2021 595:1819–1824.

6 J Med Virol. 2021 93:5409–5415.

7 Clinic Rev Allerg Immunol (2021).

8 Clin Infect Dis. 2021 Aug 18;ciab707.