Figure 1.
Lack of granulation tissue formation in MGL1-deficient mice. (A-J) Samples of inflamed skin covering the dorsal air pouch were collected on day 4 from wild-type (WT) or MGL1-deficient (KO) mice. Frozen sections were prepared and stained with hematoxylin and eosin (H.E.), with mAb LOM-14 that is reactive with both MGL1 and MGL2, with mAb LOM-8.7 that is reactive only with MGL1, and with mAb URA-1 that is reactive with MGL2, or mouse IgG. The binding of mAbs was immunohistochemically detected using biotin anti–rat κ/λ mAb plus alkaline phosphatase-streptavidin. (K) Specimens of inflamed skin covering the dorsal air pouch were collected on days 4, 11, and 18. The thickness of the granulation tissue (ordinate) was microscopically determined by measuring the hypodermis region between the muscle fiber layer and the inner surface of the air pouch. Each symbol represents the thickness of an individual wild-type mouse (open symbols) or MGL1-deficient mouse (filled symbols). Wild-type mice developed granulation tissues at the site of chronic antigenic stimulation, whereas MGL1-deficient mice did not. M represents muscle fiber layer. Bars represent 100 μm (A,B) or 10 μm (D-J). Arrows indicate positively stained cells with the mAbs. *P < .05, **P < .001.