Staining intensity was high (+++) i

Staining intensity was high (+++) in the supporting cells of the hypertrophied sebaceous acini (Figure 6),
which would suggest a high-level expression. In the pilosebaceous
follicle, in the infrainfundibular area, dyskeratotic,
vacuolated keratinocytes appear to be less stained
(+) (Figure 7). Comedones, also present in AF, showed
staining for cytokeratins only in the follicular wall
(Figure 8). Macrophages in the perifollicular dermis had
specific receptors able of being activated by P. acnes,
amplifying the inflammatory reaction.
In AF, the dermal perifollicular inflammatory infiltrate
was dominated by CD3+ cells (T-lymphocytes) and
CD68+ cells (of the mononuclear phagocyte system)
(Figure 9), fact supporting the hypothesis of the involvement
of delayed hypersensitivity reaction (type IV)
in the pathogenesis of acne. CD3+ cells accounted for
40–50% of all cells in the perifollicular inflammatory
infiltrates.
CD68+ macrophages were present in all cases of acne
studied, regardless of the type of inflammatory lesion.
Their number was higher in AF, being located in the close
vicinity of dilated and broken follicle wall, and some
of them presenting as epithelioid cells and giant cells,
additional argument supporting the cell-mediated hypersensitivity
as a major pathogenic mechanism in acne.
Together with lymphocytes and neutrophils, they might
constitute the foreign body granulomatous reaction.
CD20+ cells (B-lymphocytes) (Figure 10) were found
in small numbers and only in the severe forms of acne,
including AF (less than 20 cells in the entire inflammatory
infiltrate).
Chronic inflammatory inflammation, characteristic to
acne lesions, was also accompanied by angiogenesis. By
specific immunostaining for CD34+ endothelial cells, our
study revealed the presence of blood capillaries around
the pilosebaceous follicles, within the inflammatory or
pericystic infiltrate (Figure 11).

Results (Indonesian) 1:

Staining intensity was high (+++) in the supporting cells of the hypertrophied sebaceous acini (Figure 6),which would suggest a high-level expression. In the pilosebaceousfollicle, in the infrainfundibular area, dyskeratotic,vacuolated keratinocytes appear to be less stained(+) (Figure 7). Comedones, also present in AF, showedstaining for cytokeratins only in the follicular wall(Figure 8). Macrophages in the perifollicular dermis hadspecific receptors able of being activated by P. acnes,amplifying the inflammatory reaction.In AF, the dermal perifollicular inflammatory infiltratewas dominated by CD3+ cells (T-lymphocytes) andCD68+ cells (of the mononuclear phagocyte system)(Figure 9), fact supporting the hypothesis of the involvementof delayed hypersensitivity reaction (type IV)in the pathogenesis of acne. CD3+ cells accounted for40–50% of all cells in the perifollicular inflammatoryinfiltrates.CD68+ macrophages were present in all cases of acnestudied, regardless of the type of inflammatory lesion.Their number was higher in AF, being located in the closevicinity of dilated and broken follicle wall, and someof them presenting as epithelioid cells and giant cells,additional argument supporting the cell-mediated hypersensitivityas a major pathogenic mechanism in acne.Together with lymphocytes and neutrophils, they mightconstitute the foreign body granulomatous reaction.CD20+ cells (B-lymphocytes) (Figure 10) were founddalam jumlah kecil dan hanya dalam bentuk parah jerawat,termasuk AF (kurang dari 20 sel di seluruh inflamasimenyusup).Peradangan inflamasi kronis, karakteristik untuklesi jerawat, itu juga disertai oleh angiogenesis. OlehKhusus immunostaining untuk CD34 + sel-sel endotel, kamiStudi mengungkapkan adanya kapiler darah di sekitarfolikel pilosebaceous, dalam peradangan ataupericystic menyusup (Gambar 11).

Results (Indonesian) 2:

Intensitas pewarnaan tinggi (+++) dalam sel pendukung dari asinus sebaceous hipertrofi (Gambar 6),
yang akan menyarankan ekspresi tingkat tinggi. Dalam pilosebaceous
folikel, di daerah infrainfundibular, dyskeratotic,
keratinosit vakuolisasi terutama tampaknya kurang bernoda
(+) (Gambar 7). Komedo, juga hadir dalam AF, menunjukkan
pewarnaan untuk cytokeratins hanya di dinding folikel
(Gambar 8). Makrofag dalam dermis perifollicular memiliki
reseptor spesifik mampu dari yang diaktifkan oleh P. acnes,
memperkuat reaksi inflamasi.
Dalam AF, dermal perifollicular infiltrat inflamasi
didominasi oleh CD3 + sel (T-limfosit) dan
CD68 + sel (sistem mononuklear fagosit)
(Gambar 9), fakta yang mendukung hipotesis dari keterlibatan
tertunda reaksi hipersensitivitas (tipe IV)
dalam patogenesis jerawat. CD3 + sel menyumbang
40-50% dari semua sel dalam inflamasi perifollicular
infiltrat.
CD68 + makrofag hadir dalam semua kasus jerawat
dipelajari, terlepas dari jenis lesi inflamasi.
Jumlah mereka lebih tinggi pada AF, yang terletak di dekat
sekitar melebar dan dinding folikel yang rusak, dan beberapa
dari mereka menyajikan sel epiteloid dan sel raksasa,
argumen tambahan mendukung hipersensitivitas yang diperantarai sel
sebagai mekanisme patogenik utama dalam jerawat.
Bersama dengan limfosit dan neutrofil, mereka mungkin
merupakan benda asing granulomatosa reaksi.
CD20 + sel (B-limfosit) (Gambar 10) yang ditemukan
dalam jumlah kecil dan hanya dalam bentuk parah jerawat,
termasuk AF (kurang dari 20 sel di seluruh inflamasi
menyusup).
peradangan inflamasi kronis, karakteristik untuk
jerawat lesi, juga disertai oleh angiogenesis. Dengan
immunostaining khusus untuk CD34 + sel endotel, kami
studi mengungkapkan adanya kapiler darah di sekitar
folikel pilosebaceous, dalam inflamasi atau
pericystic menyusup (Gambar 11).