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Stephen Man

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Table 2. Reported studies of human CD4+ T cells that are specific for human papillomavirus types 16 and 18 (HPV-16, HPV-18) (tab002smc)
Study and assay detailsa Comments
(Ref. 30) Cubie et al. (1989)
Antigen: HPV-16 E6 protein; HPV-18 E6 protein; HPV-16 E4 protein.
T-cell responses: Women with CIN: 8/29. Controls: 3/15.		 Low responses in T cells. No significant difference in T-cell responses between patients and controls. HPV types of patients not known. No specificity controls. No HPV typing.
(Ref. 31) Altmann et al. (1992)
Antigen: HPV-16 E7 protein. HPV-16 E7 peptides.
T-cell responses: HPV-16+ controls: 2/3. HPV-16- controls: 0/2Controls: 2/3.		 Normal donors only, who were either seropositive or negative for HPV-16 E4 and E7. CD4 T-cell clones isolated. Peptide epitopes were defined using pooled peptides. A fusion protein control (for GST) was used.
(Ref. 32) Strang et al. (1990)
Antigen: HPV-16 E6 peptides. HPV-16 L1 peptides.
T-cell responses: Several controls tested.		 Normal donors only. T cells were HLA-DR restricted and HPV-16 specific.
(Ref. 36) Kadish et al. (1994)
Antigen: HPV-16 E7 peptides.
T-cell responses: Women with CIN: 12/42. Controls: 3/13.		 Correlation between ongoing HPV infection and T-cell responses. 9/25 women who had CIN and were infected with HPV made a T-cell response compared with 3/17 women who had CIN and were HPV-.
(Ref. 33) Luxton et al. (1996)
Antigen: HPV-16 E7 protein. HPV-16 E7 peptides.
T-cell responses: Women with CIN: 9/31. Women with CaCx: 0/5. Controls: 7/15.		 No significant difference between T-cell responses in patients and controls. No significant association between HPV-16 infection and T-cell responses in CIN patients. Decreased T-cell responses in cancer patients.
(Ref. 38) de Gruijl et al. (1996)
Antigen: HPV-16 E7 protein. HPV-16 E7 peptides.
T-cell responses: Women with CIN and HPV-16+: 15/26. Women with CIN and HPV-16-: 0/15.		 T-cell responses were most frequent in women with CIN3 who had persistent HPV-16 infection. Responses were also found in women with CIN3 who had cleared HPV-16 or had a fluctuating HPV-16 infection.
(Ref. 34) Shepherd et al. (1996)
Antigen: HPV-16 L1 peptides.
T-cell responses: Women with CIN: 26/41. Controls: 5/11.		 T-cell responses were most prevalent in the CIN3 group who had HPV-16 infection. Responding T cells were CD4+.
(Ref. 37) Kadish et al. (1997)
Antigen: HPV-16 E6 peptides. HPV-16 E7 peptides.
T-cell responses: Response to E6 peptides of women with CIN2: 32/49. Response to E7 peptides of women with CIN2: 21/48. Controls: not tested.		 T-cell responses were associated with clearance and regression of HPV-associated CIN2 lesions. Controls for PHA and ConA were present. No controls for normal donors.
(Ref. 40) de Gruijl et al. (1998)
Antigen: HPV-16 E7 peptides.
T-cell responses: Women with CIN3 and HPV-16+: 14/15. Women with CaCx and HPV-16+: 7/15.		 T-cell responses were measured only by IL-2 release. The highest frequency of responders were among women with CIN3 who had persistent HPV-16 infection. Responses were also found in women with CIN3 who had cleared HPV-16 (8/13). Decreased responses were found in women who had CaCx.

a Antigen = the antigen source used in in vitro assays to test for HPV-specific T-cell responses; T-cell responses = the numbers of people who had T cells that responded in vitro to HPV antigens and the types of people (including HPV status) who the T cells were derived from.

Abbreviations: CaCx = cervical cancer; CD4 = a cell-surface receptor that is typically found on T-helper lymphocytes; CIN = cervical intraepithelial neoplasia, including all stages (1–3); CIN2 = CIN stage 2; CIN3 = CIN stage 3; ConA = concanavalin A, a lectin used to stimulate polyclonal T cells (T lymphocytes); E4, E6, E7, L1 = HPV proteins (E = early, L = late); HLA-DR = a type of human leucocyte antigen, which is one of the human forms of the major histocompatibility complex (MHC) class II; IL-2 = interleukin 2; PHA = phytohaemagglutinin, a lectin used to stimulate polyclonal T cells.

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